A Dissertation on
A STUDY ON ASSOCIATION BETWEEN ANTHROPOMETRIC AND LIPID PARAMETERS IN NEWLY DIAGNOSED TYPE 2
DIABETES MELLITUS PATIENTS
Dissertation Submitted to
THE TAMILNADU Dr.M.G.R. MEDICAL UNIVERSITY CHENNAI - 600 032
With partial fulfillment of the regulations For the award of the degree of M.D. GENERAL MEDICINE
BRANCH-I
COIMBATORE MEDICAL COLLEGE COIMBATORE
APRIL 2019
CERTIFICATE
Certified that this is the bonafide dissertation done by Dr. D.MANOJ and submitted in partial fulfilment of the requirements for the Degree of M.D., General Medicine, Branch I of The Tamilnadu Dr.M.G.R. Medical University, Chennai.
Date: GUIDE & PROFESSOR 3RD UNIT
DR. M.RAVEENDRAN M.D
Date:
HOD & PROFESSOR
DR. KUMAR NATARAJAN M.D
Date: THE DEAN
DR.S.ASOKAN M.S., M.Ch
COIMBATORE MEDICAL COLLEGE
DECLARATION
I solemnly declare that the dissertation titled ―A STUDY ON ASSOCIATION BETWEEN ANTHROPOMETRIC AND LIPID PARAMETERS IN NEWLY DIAGNOSED TYPE 2 DIABETES MELLITUS PATIENTS”
was done by me from JUNE 2017 to JUNE 2018 under the guidance and supervision of Professor DR.M.RAVEENDRAN M.D. This dissertation is submitted to The Tamilnadu Dr.M.G.R. Medical University towards the partial fulfilment of the requirement for the award of MD Degree in General Medicine (Branch I).
Place: Coimbatore Dr. D. MANOJ
Date:
ACKNOWLEDGEMENT
I wish to express my sincere thanks to our respected Dean Dr. B. ASOKAN M.S., MCH for having allowed me to conduct this study in our hospital.
I express my heartfelt thanks and deep gratitude to the Head of the Department of Medicine Professor. Dr. KUMAR NATARAJAN, M.D. for his generous help and guidance in the course of the study.
I express my heartfelt thanks and deep gratitude to my guide PROF.DR.M.RAVEENDRAN.M.D for her support and guidance for the study.
I sincerely thank all professors and Asst. Professors- Dr. P.S. MANSHUR, Dr.P. SANBAKASREE, Dr. K. SANGEETHA for their guidance and kind help.
My sincere thanks to Department of BIOCHEMISTRY for their help. My sincere thanks to all my friends and post-graduate colleagues for their whole hearted support and companionship during my studies.
I thank all my PATIENTS, who formed the backbone of this study without whom this study would not have been possible.
Lastly, I am ever grateful to the ALMIGHTY GOD for always showering His blessings on me and my family.
DATE: Dr. D. MANOJ
CERTIFICATE – II
This is to certify that this dissertation work titled ―A STUDY ON ASSOCIATION BETWEEN ANTHROPOMETRIC AND LIPID PARAMETERS IN NEWLY DIAGNOSED TYPE 2 DIABETES MELLITUS PATIENTS” of the candidate DR.D.MANOJ with registration Number 201611306 for the award of M.D in the branch of General Medicine I personally verified the urkund.com website for the purpose of plagiarism check. I found that the uploaded thesis file contains from introduction to conclusion pages and result shows 7%of plagiarism in the dissertation.
Guide & Supervisor sign with Seal.
TABLE OF CONTENTS
S. No. CONTENT Page No.
1 AIMS AND OBJECTIVES 1
2 INTRODUCTION 2
3 REVIEW OF LITERATURE 4
4 LIST OF ABBREVIATIONS 33
5 MATERIALS AND METHODS 34
6 OBSERVATIONS AND RESULTS 36
7 DISCUSSION 77
8 SUMMARY 81
9 CONCLUSION 82
10 BIBLIOGRAPHY 83
11 ANNEXURES
I. PROFORMA II. MASTER CHART
III. KEY TO MASTER CHART IV. CONSENT FORM
88 90 94 95
LIST OF TABLES
SL.NO TABLE TITLE PAGE
NO
1 AGE DISTRIBUTION 36
2 SEX DISTRIBUTION 37
3 LIPID PROFILE 38
4 MEAN CHOLESTEROL BASED ON SEX 39
5 MEAN TRIGLYCERIDE BASED ON SEX 40
6 MEAN HDL-CHOLESTEROL BASED ON SEX 41
7 MEAN LDL-CHOLESTEROL BASED ON SEX 42
8 DISTRIBUTION BASED ON BODY WEIGHT 43
9 COMPARISON BETWEEN BMI AND TOTAL CHOLESTEROL
44
10 COMPARISON BETWEEN BMI AND TRIGLYCERIDE
45
11 COMPARISON BETWEEN BMI AND HDL- CHOLESTEROL
46
12 COMPARISON BETWEEN BMI AND LDL- CHOLESTEROL
47
13 DISTRIBUTION BASED ON WAIST CIRCUMFERENCE
48
14
COMPARISON BETWEEN WAIST CIRCUMFERENCE AND TOTAL CHOLESTEROL
49
15 COMPARISON BETWEEN WAIST
CIRCUMFERENCE AND TRIGLYCERIDE
50
16
COMPARISON BETWEEN WAIST CIRCUMFERENCE AND HDL- CHOLESTEROL
51
17
COMPARISON BETWEEN WAIST CIRCUMFERENCE AND LDL- CHOLESTEROL
52
18 DISTRIBUTION OF WAIST HIP RATIO 53
19 COMPARISON OF WAIST HIP RATIO AND TOTAL CHOLESTEROL
54
20 COMPARISON OF WAIST HIP RATIO AND TRIGLYCERIDE
55
21 COMPARISON OF WAIST HIP RATIO AND HDL-CHOLESTEROL
56
22 COMPARISON OF WAIST HIP RATIO AND LDL-CHOLESTEROL
57
23 COMPARISON BETWEEN FASTING BLOOD SUGAR AND SYSTOLIC BP
58
24 COMPARISON BETWEEN POSTPRANDIAL BLOOD SUGAR AND SYSTOLIC BP
59
25 COMPARISON BETWEEN FASTING BLOOD SUGAR AND DIASTOLIC BP
60
26 COMPARISON BETWEEN POSTPRANDIAL BLOOD SUGAR AND DIASTOLIC BP
61
27
COMPARISON BETWEEN WAIST
CIRCUMFERENCE AND FASTING BLOOD SUGAR
62
28
COMPARISON BETWEEN WAIST
CIRCUMFERENCE AND POSTPRANDIAL BLOOD SUGAR
63
29 COMPARISON BETWEEN WAIST HIP RATIO AND FASTING BLOOD SUGAR
64
30 COMPARISON BETWEEN WAIST HIP RAIO AND POSTPRANDIAL BLOOD SUGAR
65
31
COMPARISON BETWEEN TOTAL
CHOLESTEROL AND FASTING BLOOD SUGAR
66
32
COMPARISON BETWEEN TOTAL CHOLESTEROL AND POSTPRANDIAL BLOOD SUGAR
67
33 COMPARISON BETWEEN TRIGLYCERIDE AND FASTING BLOOD SUGAR
68
34 COMPARISON BETWEEN TRIGLYCERIDE AND POST PRANDIAL BLOOD SUGAR
69
35
COMPARISON BETWEEN HDL-
CHOLESTEROL AND FASTING BLOOD SUGAR
70
36
COMPARISON BETWEEN HDL-
CHOLESTEROL AND POST PRANDIAL BLOOD SUGAR
71
37
COMPARISON BETWEEN LDL-
CHOLESTEROL AND FASTING BLOOD SUGAR
72
38
COMPARISON BETWEEN LDL-
CHOLESTEROL AND POST PRANDIAL BLOOD SUGAR
73
39 COMPARISON BETWEEN BODY MASS INDEX AND FASTING BLOOD SUGAR
74
40
COMPARISON BETWEEN BODY MASS INDEX AND POST PRANDIAL BLOOD SUGAR
75
LIST OF CHARTS
SL.NO CHART TITLE PAGE
NO
1 AGE DISTRIBUTION 36
2 SEX DISTRIBUTION 37
3 LIPID PROFILE 38
4 MEAN CHOLESTEROL BASED ON SEX 39
5 MEAN TRIGLYCERIDE BASED ON SEX 40
6 MEAN HDL-CHOLESTEROL BASED ON SEX 41
7 MEAN LDL-CHOLESTEROL BASED ON SEX 42
8 DISTRIBUTION BASED ON BODY WEIGHT 43
9 COMPARISON BETWEEN BMI AND TOTAL CHOLESTEROL
44
10 COMPARISON BETWEEN BMI AND TRIGLYCERIDE
45
11 COMPARISON BETWEEN BMI AND HDL- CHOLESTEROL
46
12 COMPARISON BETWEEN BMI AND LDL- CHOLESTEROL
47
13 DISTRIBUTION BASED ON WAIST CIRCUMFERENCE
48
14
COMPARISON BETWEEN WAIST CIRCUMFERENCE AND TOTAL CHOLESTEROL
49
15 COMPARISON BETWEEN WAIST
CIRCUMFERENCE AND TRIGLYCERIDE
50
16
COMPARISON BETWEEN WAIST CIRCUMFERENCE AND HDL- CHOLESTEROL
51
17
COMPARISON BETWEEN WAIST CIRCUMFERENCE AND LDL- CHOLESTEROL
52
18 DISTRIBUTION OF WAIST HIP RATIO 53
19 COMPARISON OF WAIST HIP RATIO AND TOTAL CHOLESTEROL
54
20 COMPARISON OF WAIST HIP RATIO AND TRIGLYCERIDE
55
21 COMPARISON OF WAIST HIP RATIO AND HDL-CHOLESTEROL
56
22 COMPARISON OF WAIST HIP RATIO AND LDL-CHOLESTEROL
57
23 COMPARISON BETWEEN FASTING BLOOD SUGAR AND SYSTOLIC BP
58
24 COMPARISON BETWEEN POSTPRANDIAL BLOOD SUGAR AND SYSTOLIC BP
59
25 COMPARISON BETWEEN FASTING BLOOD SUGAR AND DIASTOLIC BP
60
26 COMPARISON BETWEEN POSTPRANDIAL BLOOD SUGAR AND DIASTOLIC BP
61
27 COMPARISON BETWEEN WAIST
CIRCUMFERENCE AND FASTING SUGAR
62
28
COMPARISON BETWEEN WAIST
CIRCUMFERENCE AND POSTPRANDIAL BLOOD SUGAR
63
29 COMPARISON BETWEEN WAIST HIP RATIO AND FASTING BLOOD SUGAR
64
30 COMPARISON BETWEEN WAIST HIP RAIO AND POSTPRANDIAL BLOOD SUGAR
65
31
COMPARISON BETWEEN TOTAL
CHOLESTEROL AND FASTING BLOOD SUGAR
66
32
COMPARISON BETWEEN TOTAL CHOLESTEROL AND POSTPRANDIAL BLOOD SUGAR
67
33 COMPARISON BETWEEN TRIGLYCERIDE AND FASTING BLOOD SUGAR
68
34 COMPARISON BETWEEN TRIGLYCERIDE AND POST PRANDIAL BLOOD SUGAR
69
35
COMPARISON BETWEEN HDL-
CHOLESTEROL AND FASTING BLOOD SUGAR
70
36
COMPARISON BETWEEN HDL-
CHOLESTEROL AND POST PRANDIAL BLOOD SUGAR
71
37
COMPARISON BETWEEN LDL-
CHOLESTEROL AND FASTING BLOOD SUGAR
72
38
COMPARISON BETWEEN LDL-
CHOLESTEROL AND POST PRANDIAL BLOOD SUGAR
73
39 COMPARISON BETWEEN BODY MASS INDEX AND FASTING BLOOD SUGAR
74
40
COMPARISON BETWEEN BODY MASS INDEX AND POST PRANDIAL BLOOD SUGAR
75
1
AIMS AND OBJECTIVES OF STUDY
1. To study the occurrence of dyslipidaemia in newly detected type2 diabetes mellitus
2. To study the pattern of dyslipidaemia in this group
3. To assess the relationship between anthropometric measurements and dyslipidaemia
2
INTRODUCTION
Diabetes Mellitus (DM) is a chronic disease and a silent epidemic.
Recent estimates show that by 2030, number of people with diabetes will increase to more than 366 million which is twice the number in 2000. Diabetes is more prevalent in developing countries and India is becoming the diabetic capital in the world with prevalence range next to China. India has around 69.1 million people with diabetes. The increased prevalence is attributed to ageing of the population and obesity. Type 2 diabetes being a chronic disease is characterized by hyperglycaemia and dyslipidaemia due to underlying insulin resistance. As the disease progresses it leads to micro vascular and macro vascular complications. Obesity and particularly abdominal obesity are strongly associated with insulin resistance. The aetiology of diabetes is attributed to environmental and genetic factors. The modifiable risk factors like abdominal obesity and physical inactivity are major contributors to the disease.
Rapid lifestyle changes, other non-communicable diseases like hypertension, dyslipidaemia are also major etiologic factors for the rising incidence of type 2 diabetes around the globe. The Body Mass Index (BMI), Waist to Hip Ratio (WHR), and the Waist Circumference (WC) are three main anthropometric parameters to evaluate body fat and fat distribution in adults. These parameters vary between the different ethnic populations. Previous studies have shown that BMI and WHR can predict outcome of diabetes and WC correlates better with intraabdominal fat than WHR. In Indian population central obesity is more common in diabetic patients, hence their influence on diabetes and its
3
complications gains importance. So Waist Circumference and Waist Hip Ratio are better predictors of obesity than Body Mass Index in Indian population.
Patients with type 2 diabetes mellitus-associated dyslipidaemia have a high risk of cardiovascular diseases and its complications. The lipid parameters serum Cholesterol, serum Triglyceride, serum Low Density Lipoprotein (LDL), serum High Density Lipoprotein(HDL) are correlated with blood sugar levels in this study. An understanding of the complex interplay of how treating dyslipidaemia reduces the risk for CVD events in patients with type 2 diabetes mellitus and an ability to assess at-risk patients is necessary to ensure the most appropriate treatment strategies are implemented. The aim of this study was to quantify the association between three anthropometric measurements (body mass index, waist to hip ratio, waist circumference) and lipid profilein newly detected type 2 diabetes mellitus patients.
4
REVIEW OF LITERATURE
Diabetes mellitus is a disease which affects all age group and is a vascular disease that affects the endothelium all over the body. Diabetes mellitus is recognized as a syndrome, a collection of disorders that have hyperglycemia and glucose intolerance as their hallmark which can be due either to insulin deficiency or to impaired effectiveness of insulin’s action or both.
Etiological Classification of Hyperglycaemia (WHO 1999): (1)
Type 1 Diabetes mellitus (β-cell destruction, usually leading to absolute insulin deficiency)
Autoimmune Idiopathic
Type 2 Diabetes mellitus (may range from predominantly insulin resistance with relative insulin deficiency to a predominantly secretory defect with or without insulin resistance)
Other specific types
Genetic defects of β-cell function
Genetic defects in insulin action
Diseases of the exocrine pancreas
Endocrinopathies
Drug- or chemical-induced
5
Infections
Uncommon forms of immune-mediated diabetes
Other genetic syndromes sometimes associated with diabetes Gestational diabetes
The terms insulin-dependent diabetes mellitus and non-insulin dependent diabetes mellitus were removed from classification of diabetes because it classified based on age and treatment given only and pathogenesis of the disease was not considered. The current classification retains the terms ―type 1‖
and ―type 2‖ diabetes mellitus (Arabic numerals are used). Type 1 diabetes mellitus occurs due to autoimmune process leading to β-cell destruction but the pathogenesis and etiology are not known. The conditions like e.g. cystic fibrosis; mitochondrial defects which have specific etiologies for beta cell dysfunction are not classified as type 1diabetes. Type 2 diabetes mellitus is due to defective insulin secretion and/or from insulin resistance or combination of both. Malnutrition related diabetes (MRDM) is removed from the WHO classification (2). It has two subtypes. One of which is protein-deficient pancreatic diabetes needs a better definition. Next is fibrocalculous pancreatic diabetes (FCPD) which is classified as a disease of the exocrine pancreas and named as ―fibrocalculous pancreatopathy‖, which can lead to diabetes.
6
Other Specific Types of Diabetes: (3) Genetic defects of 𝛃-cell
function
HNF1A MODY HNF4A MODY HNF1B MODY GCK MODY
MtDNA 3243 MIDD KCNJ11 PNDM KCNJ11 DEND 6q24 TNDM ABCC8 TNDM INS PNDM
WFS1 Wolfram syndrome FOXP3 IPEX syndrome EIF2AK3 Wolcott–
Rallison syndrome
Genetic defects in insulin action
INSR Type A insulin resistance
INSR Leprechaunism INSR Rabson–Mendenhall syndrome
LMNA FPLD PPARG FPLD AGPAT2 CGL BSCL CGL
Lipoatrophic diabetes
Diseases of the exocrine pancreas
Fibrocalculouspancreatopathy Pancreatitis
Trauma / pancreatectomy Neoplasia
Cystic fibrosis Hemochromatosis Others
Endocrinopathies Cushing syndrome Aldosteronoma Acromegaly
Pheochromocytoma Glucagonoma Hyperthyroidism Somatostatinoma Others
Drug- or chemical- induced
Nicotinic acid Glucocorticoids Thyroid hormone
Alpha-adrenergic agonists Beta-adrenergic agonists Thiazides
Dilantin Pentamidine Vacor
Interferon-alpha therapy Statins
L-asparagine
Antipyschotic drugs, e.g.
clozapine,
Highly active antiviral therapy, e.g. protease inhibitors
Others
Infections
Congenital rubella Cytomegalovirus Others
7 Uncommon forms of
immune-mediated diabetes
Insulin autoimmune syndrome (antibodies to insulin)
Anti–insulin receptor antibodies
―Stiff man‖ syndrome Others
Other genetic syndromes Down syndrome
Friedreich’s ataxia Huntington’s chorea Klinefelter syndrome Lawrence–Moon–Biedl syndrome
Myotonic dystrophy Porphyria
Prader–Willi syndrome Turner syndrome Wolfram syndrome
Diagnosis:
Diagnosis is established by demonstration of elevated blood sugar levels. It includes random blood sugar, fasting and postprandial blood sugar and OGTT of 75 grams for testing. For children, the oral glucose load is 1.75 g per kg body weight. HbA1c is also a reliable means of diagnosing diabetes recommended by the ADA and WHO.
HbA1c (Glycosylated Hemoglobin)
HbA1c is a hemoglobin variant formed by the nonenzymatic attachment of glucose to hemoglobin. HbA1c has become the cornerstone marker for monitoring of diabetic patients.HbA1c measurements are done using standardized assays. Maintaining HbA1c levels within normal range is important in reducing the risk of micro vascular complications of diabetes.
HbA1c levels predict diabetic retinopathy and macro vascular event mortality.
Advantages of using it include daily variation is not a problem, sample drawn
8
will be stable for at least one week, patient does not require fasting and its reflects blood sugar control for 3 to 4 months. The disadvantage in HbA1c is conditions that alter the red cell turnover and cost of the assay. The cutoff for HbA1c to diagnose diabetes by WHO is level more than or equal to 6.5% (4).
But diagnosis of diabetes using HbA1c will underestimate the prevalence of diabetes. Type 2 diabetes mellitus is a threat to human health in the twenty-first century. Estimates show that by 2025, around 300 million people will have diabetes with expected 70% increase in developing countries.
The prevalence of diabetes among Asian populations especially in Indian men and women increases with age up to 60s and then declines. The prevalence of diabetes were higher in people of India and Singapore than in most of the Chinese and Japanese people in DECODA study (5). In India there was 10% prevalence among people in 40–49 years age group, 30% in 50–69 years age group. The ratio of prevalence of blood glucose abnormality does not show a consistent trend. In the age group of 30 to 69 years, undiagnosed diabetes and impaired glucose tolerance (IGT) is more common in men. Post prandial hyperglycemia is more common in elderly men.
American Diabetes Association (ADA) Classification of DM:
Four criteria for diagnosis of diabetes mellitus:
1) Glycated hemoglobin (A1C) value of 6.5% or higher 2) Fasting plasma glucose more than 126 mg/dl (7.0 mmol/ l)
9
3) 2 hour plasma glucose more than 200 mg/dl (11.1 mmol/l) During OGTT done with 75 gram of glucose
4) Classic symptoms of hyperglycemia- polyuria, polydipsia, and unexplained weight loss or hyperglycemic crisis with a random plasma glucose of 200 mg/dl (11.1 mmol/l) or higher.
Glucose use and insulin action:
Glucose concentration in plasma is 15% higher than in whole blood and arterial blood sugar levels are highest when compared to venous and capillary blood sugar levels. Glucose transport between tissues occurs through plasma and RBCs. Insulin dependent tissues include brain, liver, kidney, intestine, and placenta. Uptake of glucose is mediated by tissue-specific glucose transporters (GLUTs) that occurs in both insulin-sensitive tissues and insulin-insensitive tissues. Insulin mediated vasodilatation can retain more glucose for use in the muscles. During fasting, glucose uptake of insulin independent tissues occurs and two thirds of the glucose is oxidized. Brain uses glucose as a fuel (5).
Insulin dependent tissues use fat as a fuel during fasting and more than fifty percent of basal energy production is relied on fat oxidation.
The liver (hepatic glucose production) is more sensitive to inhibition by insulin than the stimulation action by insulin on the peripheral tissues (glucose uptake). Insulin acts on glucose metabolism by direct and indirect mechanisms.
10
DIRECT ACTIONS INDIRECT ACTIONS Enhancement of glucose transport
glycolytic breakdown & incorporation into glycogen
Inhibition of lipolysis, Lipid oxidation &
Protein degradation
Tissues sensitive to insulin have glucose, FFA and amino acids competing with each other and the effect of counter regulatory hormones is opposing the effects of insulin.
Physiologic hyperinsulinemia activates the insulin signal transduction system leading to a coordinated increase in glucose transport/phosphorylation, glycogen synthesis, and glucose oxidation. Insulin suppresses endogenous glucose production and promotes glucose uptake into muscle in response to oral glucose load. GLP-1 by its direct effects and indirect actions of increasing insulin and inhibition of glucagon causes glucose uptake in liver cells and inhibits glucose production by liver (6).
Pathogenesis of T2DM:
Type 2 diabetes is characterized by –
Muscle insulin resistance leading to decreased in glucose uptake
Hepatic insulin resistance leading to increase in glucose production
Adipocyte insulin resistance leading to increase in plasma FFA
Increased insulin resistance stimulate adipocytokine release
Progressive β-cell failure
11
Hyperglucagonemia
Increase in hepatic sensitivity to glucagon
Impaired incretin effect (GLP-1 and GIP)
Increased renal glucose reabsorption
Brain neurotransmitter dysfunction leading to failure of appetite suppression resulting in weight gain
Insulin resistance coupled with progressive beta cell failure is responsible for progression of disease from impaired glucose tolerance to overt diabetes mellitus. The most dominant feature of insulin resistance is obesity. Evidence of insulin resistance (IR) in lipid pattern is elevated triglyceride and lower HDL-cholesterol levels. These along with elevated blood pressure form the diagnostic criteria for metabolic syndrome (7). Recently elevated levels of ALT and GGT are indicative of insulin resistance. Insulin resistance is also associated with alteration in adipokines, vascular dysfunction, and immune dysregulation.
Insulin resistance:
Insulin resistance is defined as abnormal biologic response to insulin.
Insulin resistance is the key factor in the pathogenesis of T2DM. Action of insulin is on skeletal muscle, adipose tissue, liver, endothelium, and immune cells. Insulin resistance leads to hyperglycemia due to reduced muscle uptake of glucose and increased release of glucose substrates from liver (FFA).
Hyperinsulinemia occurs in response to hyperglycemia (8). This exhausts
12
pancreas which is burnt out and unable to produce sufficient insulin to maintain blood sugar levels within the normal range. This results in diabetes mellitus.
Measurement of insulin resistance:
The method for testing is called euglycemichyperinsulinemic clamp.
This technique measures insulin resistance in the presence of hyperinsulinemic state the ability to maintain normal blood glucose levels. Glucose is infused at a rate sufficient to maintain euglycemia and insulin is infused at supraphysiological rates (9). The role of muscle and adipose tissue is tested using stable isotopes. After achieving steady state, the rate of glucose infusion predicts ability of tissue to respond to insulin and tissue take up of glucose for a standard insulin dosing. This technique is considered gold standard but it is time consuming and difficult in routine measurements and cannot be followed in large epidemiologic studies. The risk factors for prediction of T2DM include
—age, gender, measures of adiposity, family history of T2DM, and ethnicity.
Insulin Resistance and Ectopic Fat:
Patients prone to T2DM accumulate visceral or ectopic fat for a given weight. This leads to impaired subcutaneous fat storage capacity. One entity is lipodystrophy in which there is accumulation of fat in ectopic tissues and insulin resistance. The location of fat storage places a role in BMI and development of metabolic complications of insulin resistance.
13 Pancreas Morphology and Diabetes:
Islet β-cell volume is decreased in T2DM and in impaired fasting glucose. There is a relative increase in the α: β cell ratio. Early in the course of hyperglycemia there is distortion of islet capillary morphology and as the disease progresses there is loss of capillary density and associated islet cell fibrosis (10). The various mechanisms that lead to beta cell loss include elevated glucose and free fatty acids, amyloid deposition in islet cells and inflammation of islet cells.
Chronically elevated glucose and/or free fatty acids:
Chronic exposure of β cells to elevated glucose results in impaired β-cell function due to oxidative stress and activation of Fas receptor-mediated or mitochondrial apoptosis. Exposure of β cells to increased free fatty acids (FFA) with associated hyperglycemia can lead to impairment of insulin release. They also cause beta cell apoptosis. Excess nutrients are thus detrimental to β-cell secretory function.
Amyloid deposition in islet cells:
Found in patients with T2DM also in cystic fibrosis-related diabetes.
Accumulation of islet amyloid occurs due to aggregation of the normally solublebeta cell peptide IAPP that gets deposited in the extracellular matrix which lies between islet capillaries and β cells. Amyloid deposition is associated with decreased β-cell volume increase in β-cell apoptosis. Amyloid- induced oxidative stress and increased β-cell apoptosis via activation of the cell
14
surface death receptor Fas or cJun N-terminal kinase (JNK) and that leads to downstream activation of apoptosis. IAPP aggregation is an important mediator of β-cell toxicity (11). IAPP deposition leads to stress response of ER (endoplasmic reticulum). IAPP deposition occurs when its plasma levels are very high. Also IAPP is proinflammatory that elicits a cytokine and chemokine production from the macrophages/dendritic cells.
Inflammation of islet cells:
Islet cell inflammation is a hallmark finding in T1DM due to release of proinflammatory cytokines that lead to beta cell infiltration and lead to beta cell death. In T2DM there is low-grade, chronic inflammation that is associated with insulin resistance. Increased production of interleukin 1β in response to chronic high blood glucose levels by the beta cells can activate signaling pathways of innate immune response. This leads to β-cell toxicity and death.
Risk factors for type 2 diabetes mellitus:
The risk factors for type 2 diabetes mellitus includes the modifiable and non-modifiable risk factors. Weight gain, obesity and physical inactivity are one of the important modifiable risk factors.
Obesity:
Obesity occurs when there is mismatch between energy intake and energy expenditure. BMI is the weight of a person in kilograms divided by square of height in meters. Studies have reported that one unit raise in BMI is
15
associated with 12% increased risk of T2DM. Another entity coming up in recent years is lean diabetes (12). This form of diabetes occurring in young males deprived of nutrition in childhood coming from a poor socioeconomic status with onset of disease at early age without ketosis. These patients have high incidence of beta cell failure. This entity having a multifactorial causation due to genetic, environmental and behavioral factors with increased risk of cardiovascular mortality. Talking about the influence of obesity per se- central obesity which is deposition of adipose tissue in trunk and abdominal area is a strong risk factor for diabetes mellitus. The surrogate measures of central obesity are waist circumference (WC), waist-to-hip ratio (WHR), and waist-to- thigh ratio (WTR). Subcutaneous and intraabdominal fat can also be measured using recent techniques like DEXA, MRI and CT. Intraabdominal fat alone can lead to insulin resistance not taking into account the total body fat (13).
Physical Activity:
Physical activity is defined as bodily movement that increases energy expenditure that is produced by contraction of skeletal muscle. Exercise on the other hand is defined as a subset of physical activity (PA) which is done intending physical fitness. Risk of diabetes is inversely proportional to PA. PA has an independent effect of reducing the body weight and thereby reduces risk of obesity. Exercise can also lead to improvement in insulin sensitivity. Studies have shown that when considering the duration and the amount of exercise the duration of exercise is an important determinant for reducing risk of diabetes.
16 Sedentary Lifestyle:
Sedentary lifestyle is a risk factor for both diabetes and obesity. Leisure sedentary behavior and television watching are greater in those who develop diabetes when compared with those who did not develop diabetes mellitus.
This shows positive association between increased risk of diabetes and sedentary lifestyle (33). Sedentary behavior is associated with adiposity, adiposity-associated inflammation and reduced lipoprotein lipase activity, clearance of triglycerides, clearance of an oral glucose load, and glucose- stimulated insulin secretion. Lifestyle interventions like Diabetes Prevention Program (DPP) are beneficialinimprovingglucosemetabolism. Weight loss is brought by caloric reduction but maintenance of weight loss is brought by physical activity (PA). Prolonged television (TV) watching is a surrogate of a sedentary lifestyle and a risk factor for diabetes. Spending 2–10 hours in television has 66% higher risk of diabetes and risk increases if total duration is more than 40 hours per week. There is also 23% increase in risk of obesity (14). For every 2 hour increment in sitting at work there is 5% increase in risk of diabetes mellitus. Following an active lifestyle in the form of brisk walking at least 30 to 45 min in a day 5 times in a week and watching television less than 10 hours per week can reduce the risk of new onset of diabetes by 43%.
Moderate physical activity reduces the progression of IGT (impaired glucose tolerance) to diabetes mellitus by 30–58%.
17 Dietary factors:
Diet is a phenomenon that varies based on personal preference, cultural heritage and socioeconomic factors and is made of complex interactions of numerous foods and nutrients. Measurement of diet is through food diaries and questionnaires. Diet is assessed based on absolute intake of nutrients, nutrient intake as a percentage of total energy, dietary patterns, and bioavailability characteristics of foods like glycemic index.
Dietary fat:
High-fat diet is associated with obesity. Mechanisms involved are alterations in cell membrane composition due to intake of dietary fat which alter membrane fluidity, insulin-mediated signal transduction and its action.
There is positive correlation between high-fat, low-carbohydrate diets and T2DM but the results are not consistent in all the studies (32). Specific types of fat and carbohydrate that are consumed are important. Increased intake of polyunsaturated fatty acids and long-chain n-3 fatty acids (fish oil) are beneficial and high intake of saturated fatty acids and trans-fatty acids are harmful (15).
Dietary carbohydrates:
Intake of carbohydrate poses a direct challenge to the beta cells when compared to protein or fat intake. Hence high carbohydrate diet is associated
18
with increased risk of diabetes. Composition of the carbohydrate and glycemic index of the food influence this effect.
Glycemic index:
It measures the post prandial excursion of glucose after ingestion of food. Foods with high glycemic index cause higher excursions of glucose. The postprandial excursions depend onthe rate of absorption of glucose. It also depends on type of carbohydrate(simple or complex) and the amount of fiber intake. Benefit of consuming foods with low glycemic index in reduction of risk of diabetes is not clear (16).
Other Food Intake:
High-fiber intakes is associated with reduction in risk of diabetes. But the mechanism is unknown. It can be attributed to low glycemic index of high- fiber diet. High intake of vegetables reduces the risk of diabetes. The antioxidants found in fruits like carotenoids and tocopherols associated with high fiber and vitamin intake reduce the risk of diabetes. The traditional Pima diet with high fiber and low fat diet intake has reduced incidence of DM.
Other modifiable risk factors for T2DM:
The other modifiable risk factors include inflammation and smoking.
19 Inflammation:
Inflammation is found to act as the underlying causative factor that leads to development of atherosclerosis. The marker of subclinical inflammation C- reactive protein is associated with metabolic abnormalities like obesity, insulin resistance, low HDL cholesterol and hypertriglyceridemia. Increased levels of CRP is associated with increased risk of diabetes. Thus subclinical inflammation has become an important determinant of T2DM and studies have shown that use of anti-inflammatory drugs like high-dose aspirin reduces insulin resistance and improves glucose tolerance.
Smoking:
Smoking is an independent risk factor for the development of diabetes.
Studies have shown that smoking increases risk of DM by 45% (17). Also current smokers have highest mean HbAlc concentrations and low levels are seen in non-smokers. HbAlclevels are also correlated in a dose–response manner with the number of cigarettes smoked per day and smoking measured in pack-years. Smoking is also associated with insulin resistance. Smokers have higher
Plasma triglycerides and low HDL-cholesterol levels. Oxidative stress caused by smoking induces endothelial dysfunction, resulting in insulin resistance in muscle and liver (31).
20 Anthropometry and diabetes:
Waist Circumference (WC) is recorded to the nearest 0.1 cm at level of umbilicus and hip circumference at the point of maximum diameter of thigh using an unstretched tape meter, without pressure on the body surface.
Waist-to-hip ratio (WHR) is calculated with WC divided by hip circumference. Criteria of the National Heart, Lung, and Blood Institute (NHLBI) is used to define cut-off points for central (or abdominal) obesity.
WC over 88 cm in women and over 102 cm in men is considered as a risk factor. For Waist hip ratio the cut-off points are ≥ 0.95 for men and ≥ 0.85 for women (18).
BODY MASS INDEX (BMI) is defined as the weight in kilograms divided by the square of height in meters. Globally, more than 50% diabetics have BMI above 21kg/m2.
WEIGHT STATUS BMI IN kg/m2
Underweight <18.5
Normal weight 18.5-24.9
Overweight 25-29.9
Obese ≥30
Class 1 30-34.9
Class 2 35-39.9
Class 3 ≥40
21
The anthropometric measures are used for the screening obesity, diabetes and CVD. BMI indicates generalized obesity and WC and WHR indicate central obesity. Central obesity better predicts cardiovascular risk and mortality than BMI. Also BMI and WHR are better predictors of outcome in T2DM. WC better predicts intra-abdominal fat than WHR. But which parameter is best for predicting cardiovascular events and mortality is still inconclusive (19).
Diabetes with Low Body Weight :( BMI< 18.5 kg/ m2)
There is an entity comprising of occurrence of diabetes in patients with BMI less than 18.5 which was previously called malnutrition related diabetes mellitus under subcategory termed protein deficient pancreatic diabetes.
Various other names like Jamaican type diabetes, Tropical diabetes were used but Ahuja proposed the term ―Ketosis Resistant Diabetes of the Young (KRDY)‖ which is accepted. These patients are mostly of Asian and African ethnicity (20).
Criteria for diagnosis of KRDY:
(1) Blood glucose > 200 mg%
(2) Onset < 30 years of age (3) BMI < 18 kg/m2
(4) Absence of ketosis on insulin withdrawal
(5) Poor socio-economic status or history of childhood malnutrition (6) Insulin requirement > 60 units/d or 1.5 units/kg
22
The early onset of disease and low BMI mimics TIDM but presence of islet cell specific antibodies is very less in KRDY. Studies done in India has shown that around 3.5% patients were lean diabetics and 63% have an ideal body weight at diagnosis. Micro-vascular complications of diabetes like retinopathy, nephropathy and neuropathy were more common in lean diabetics whereas hypertension and coronary artery disease are more common in the obese patients. Other factors which distinguish it from TIDM are ketosis is absent in KRDY and also KRDY patients respond to diet modification and oral antidiabetic drugs. Studies have proven that a period of malnutrition during postnatal period or early childhood can increase the risk of diabetes (21).
Studies have shown that Asian population has five-fold higher prevalence in the lean diabetes. Consumption of alcohol, cigarette smoking and pancreatitis were more among lean diabetics. They achieve poor glycemic control. The pathophysiology is rapid beta cell failure. They require insulin earlier and their TG/HDL ratio tends to be low which is considered as an indirect marker of lower insulin resistance.
The pathophysiology and its distinction from classic type 2 diabetes is still unclear (30). One difference is that peripheral insulin resistance is the key factor in T2DM which is in contrast to KRDY that shows insulin deficiency.
The fasting C-peptide levels are intermediate between type1 and type 2 diabetic patients. Though they have a small beta cell reserve which is denoted by the C- peptide levels the insulin is not available because of excessive extraction of insulin in the Porto-hepatic circulation resulting from raised glucokinase
23
activity and the hyperactive futile cycles of carbohydrate metabolism. This also explains the resistance to ketosis (22). They have lower fasting plasma FFA and ketone levels and reduced responsiveness to catechol amines that delay the development of ketoacidosis. They also have exocrine pancreatic deficiency.
A single antibody is neither sensitive nor specific to distinguish between the phenotypes of type 1 or type 2 diabetes as GAD or ICA positivity is seen in obese T2DM patients also. So the probable etiology is malnutrition combined with autoimmune process.
Obesity Paradox:
Obesity paradox is a phenomenon in which diabetes related complications and mortality were higher among diabetic population with normal weight when compared to those with obese diabetics (29). It is also observed in other conditions like heart failure, end stage renal disease and hypertension. The increased risk of death among lean diabetics who are smokers. This becomes unreliable in elderly people because of the co-existing conditions that determine mortality and unreliability of BMI as a measurement of adipose tissue mass due to age related muscle wasting and reduction in muscle mass.
Sarcopenic obesity can explain the obesity paradox. Sarcopenic obesity is defined as presence of high body fat with reduced or normal lean body mass (23). Sarcopenic obesity reduces physical fitness and cardiopulmonary functioning and lead to premature death and explains increased mortality in
24
diabetics with normal body weight. Patients with good aerobic fitness with high BMI have lower risk of mortality than those with normal BMI and poor physical fitness.
Ideal body weight is BMI between 18.5 and 24.9. Central obesity which is defined as waist circumference > 102 cm in males and> 88 cm in females defined by NCEP correlates well with the degree of insulin resistance. Chronic alcohol consumption can induce pancreatic beta cell dysfunction and cell apoptosis (24). Exposure to both passive and active smoking has positive association and is a risk factor for diabetes. Genetic defects like polymorphisms of transcription factor FL2 gene and defective ATP sensitive potassium channel can lead to defective insulin secretion. Abnormal fat distribution can also occur in type 2 diabetic patients. Both genetic and environmental factors play a role in lean diabetes.
Monogenic Diabetes Mellitus:
Monogenic β-cell diabetes accounts for 1–2% of diabetes.
25 Maturity Onset Diabetes in Young:
Maturity onset diabetes of the young (MODY) is the commonest form of monogenic β-cell diabetes in adults. It is divided into two clinical groups:
mutations in Glucokinase (GCK-MODY) and mutations in the transcription factors—HNF1A and HNF4A (TF-MODY).
Over 80% of people with MODY will initially be misdiagnosed with type 1 or type 2 DM.
26
MODY patients are not obese, lack insulin resistance and do not have autoimmune antibodies.
Diagnostic Criteria for MODY:
(i) Age of onset diabetes <25 years (ii) Non-insulin-dependent diabetes
(iii) Family history of diabetes (due to autosomal dominant inheritance) - can be absent in as much as 50% of patients.
Types of MODY:
Glucokinase MODY: (GK-MODY)
Have fasting hyperglycemia from birth but do not develop significant micro vascular complications. Treatment is not required except in pregnancy.
Transcription factor MODY: (TF-MODY)
Diabetes develops in childhood/early adult life and deteriorates. They respond to sulfonylurea treatment initially and later require insulin. Micro vascular complications are common and also CVD risk.
27
Maternally Inherited Diabetes And Deafness (MIDD): (25)
It accounts for 0.5% of diabetes. It is due to mitochondrial gene mutation producing a maternally inherited diabetes. These patients are generally non-insulin requiring but require insulin after setting of sensineural deafness.
Neonatal Diabetes:
It is diagnosed in the first six months of life. It can be transient or permanent. It results due to mutation in KATP mutation and excellent glycemic control with High-dose sulfonylurea tablets can be achieved instead of insulin injections.
Lipid and diabetes mellitus:
Diabetes mellitus patients have elevated triglyceride levels, low levels of high-density lipoprotein cholesterol, and increased small cholesteroldepleted low-density lipoproteins. The pathophysiology under diabetic dyslipidemia is insulin resistance which plays a central role in abnormal lipid and lipoprotein metabolism that occurs in T2DM.There is not much variation in cholesterol levels when compared between insulin sensitive and insulin resistant individuals. Hence assessment of CVD risk in a diabetic patient based on lipid profile should not be limited alone to total cholesterol alone. Dyslipidemia and IR is also found in prediabetics and worsens as glucose intolerance progresses (26). There is increased risk of CVD in diabetic women when compared to their male counterparts. VLDL levels increase in response to IR. IR is also
28
associated with increased levels of Apo protein B100 which is considered as the atherogenesis causing protein in the lipoprotein series and there is reduced levels of ApoA1 protein. Dyslipidemia occurs in both fasting and postprandial states. Dyslipidemia during postprandial period can lead to increased CVD risk in non-diabetic people.
Lipoprotein Metabolism:
Blood triglyceride levels are regulated by the VLDL secreted from the liver and activity of plasma lipoprotein lipases (LPL) that clear the plasma triglycerides. DM is characterized by increased release of VLDL from liver and reduced LPL activity. This leads to increased TGL levels in blood. HDL levels are low due to increased transfer of cholesterol in exchange to TGL to VLDL and LDL by CETP (cholesterol ester transfer protein). Hence the LDL particles become smaller and denser.
Lipoprotein structure:
Lipoproteinsare macromolecular complexes consisting of lipid core made of TG and cholesterylesters (CEs) anda surface made of phospholipids, free cholesterol, and one or more Apo lipoproteins. There are five distinct major classes of lipoproteins which are further divided into subclasses.
Handling of exogenous TGL is through formation of chylomicrons in the enterocyte and endogenous TGL handling is by the VLDL released from liver. VLDL, IDL and LDL require Apo B100 as their surface protein and chylomicrons requires Apo B48 which is a truncated form of Apo B100.
29
Microsomal triglyceride transfer protein (MTP) packages Apo B48 with the core lipids and forms chylomicrons. Increased intestinal expression of MTP in people with T2DM plays role in increased TGL levels. The chylomicrons enter the system through the lymphatic system and acquire Apo lipoproteins C1, C2 and C3 HDL surface. Apo C2 activates adipose tissue derived lipoprotein lipase that mediates chylomicron clearance (27). Apo C3 inhibits LPL- mediated lipolysis. The TGL from chylomicron releases free fatty acids (FFAs) which are taken by tissues and they acquire Apo E from HDL and become chylomicron remnants. These chylomicron remnants are cleared by hepatic uptake. Hepatic lipase (HL) hydrolyzes chylomicron remnant TGL and augments hepatic uptake. IR and T2DM negatively affect chylomicron remnant metabolism. Increased circulating TGL is atherogenic. Insulin targets Apo B100 for its degradation which in the presence of IR and concomitant chronic hyperinsulinemia and steatosis is decreased. Apo B 100 degradation increase ER stress that leads to VLDL secretion from liver and steatosis (28).
TGL availability is essential for VLDL assembly and secretion.
Circulating FAs from the peripheral tissues act as the main source for TGL synthesis. In case of IR and T2DM there is FAflux into the liver due to insulin resistance in adipocytes stimulate Apo lipoprotein release and TGL uptake by liver. Expression of nuclear transcription factor, peroxisome proliferator- activated receptorγ (PPARγ) is increased in T2DM, IR and hepatic steatosis.
Lipolysis of core TGLleads to formation of smaller, denser VLDL remnants referred as IDL. This process is impaired inT2DM. VLDL remnants
30
or IDL undergo further metabolic modifications to generate LDL by the action of hepatic lipase. LDLparticlesarecomposed of core CEs associated with surface Apo B100. LDL is cleared through hepatic LDL-receptor-mediated uptake. IR and uncontrolled DM is associated withreduction in LDL receptors.
LDL participates in CETP-mediated exchange of its CE with LDLorchylomicron TGL that produces small, dense LDL. The characteristic hypertriglyceridemia of T2DMis associated with presence of small, dense LDL.
Weight loss, Exercise and Diet modifications are the key to successful treatment of all of the lipid abnormalities in patients with T2DM. Statins form the main stay of treatment which lower LDL cholesterol by up to 50%, lower triglycerides by about 15–25% and have minimal effects of HDL levels.
Elevated LDL-C is a risk factor for cardiovascular morbidity and mortality.
Treatment for Dyslipidemia:
LDL-C therapy is given for four groups of patients:
1. Those with LDL-C >190mg% and those with prior CVD
2. Those with diabetes and LDL-C ≥70≤190mg% and those without CVD 3. Diabetes with LDL-C ≥70≤190mgdL−1 with risk of 10 year CVD
≥7.5%
Non-HDL-C is a surrogate marker for the Apo B100-containing lipoproteins. The new AHA/ACC guidelines has concluded that there is no evidence to target either LDL-C or non-HDL-C. ADA recommends lowering
31
TGL to less than 150mg% and maintenance of HDL-C by 40mg% in men and 50mg% in women. HDL-C is an independent predictor of CV mortality (28).
Guidelines recommend reduction in LDL-C to 30to 40% in patients more than 40 years age and reduction to less than 100mg%.
Other treatment recommendations include Medical nutrition therapy, Weight loss in overweight and obese individuals, Diet with reduced intake of total fat (∼30% of total calories), saturated fat (<7% of total calories), and trans fatty acids (minimal), cholesterol less than 200mg%, Increased exercise, Smoking cessation.
Pharmacologic therapy include statin therapy to decrease LDL-C, fibrate therapy to decrease TG and increase HDL-C and combination therapy with statin.
Metabolic Syndrome:
Reaven proposed criteria for diagnosis of metabolic syndrome which includes hypertension, dyslipidemia (specifically hypertriglyceridemia with low HDL-cholesterol), dysglycemia, and central obesity. Three out of five criteria is essential for diagnosis.
32
Elevated TGL more than 150mg% or taking drugs for hypertriglyceridemia Reduced HDL less than 40 mg% in male and 50mg% in female or drug therapy for low HDL levels
Systolic blood pressure ≥130mmHg and/or diastolic ≥85mmHg or drug therapy with a history of hypertension
Elevated fasting blood glucose more than 100mg% or glucose-lowering therapy
Abdominal obesity - WC more than 102 cm in male and more than 88 cm in females (Asian population)
33
LIST OF ABBREVATIONS
T2DM Type 2 diabetes mellitus OGTT Oral glucose tolerance test BMI Body mass index DECODA Diabetes epidemiology;
collaborative analysis of diagnostic criteria in Asia
WHR Waist to hip ratio FFA Free fatty acids
WC Waist circumference IR Insulin resistance
HDL High density lipoprotein- cholesterol
PA Physical activity
TGL Triglyceride IAPP Islet amyloid polypeptide
LDL Low density lipoprotein cholesterol
ADA American Diabetology Association
VLDL Very low density lipoprotein cholesterol
HbA1c Glycosylated haemoglobin
CVD Cardiovascular disease NCEP National cholesterol education program HNF Hepatocyte nuclear factor HL Hepatic lipase MODY Maturity onset diabetes in
young
MRDM Malnutrition related diabetes mellitus
34
MATERIALS AND METHODS
SOURCE OF STUDY: Data consists of primary data collected by the principal investigator directly from the cases of newly detected type 2 diabetes mellitus admitted in the medical ward in Coimbatore Medical College Hospital DESIGN OF STUDY: Cross sectional descriptive study
PERIOD OF STUDY: Twelve months (September 2016- September 2017) METHODOLOGY: This is a cross sectional descriptive study of 200 cases of newly detected type 2 diabetes mellitus in the medical ward of Coimbatore Medical College Hospital, Coimbatore, from September 2016 – September 2017
INCLUSION CRITERIA:
Patients fulfilling the ADA criteria for diagnosis of type 2 diabetes mellitus who are –
Newly detected type 2 diabetes mellitus Age more than 20 years
EXCLUSION CRITERIA:
1. Patients below 20 years of age 2. Acute metabolic complications 3. Diabetic ketoacidosis
4. Hyperglycaemic hyperosmolar syndrome
35 5. Acute illness
6. Acute myocardial infarction 7. Cerebrovascular accident 8. Thyroid disorders
9. Liver disorders
10. Secondary dyslipidaemia 11. Pregnancy
12. Drugs (Beta blockers, thiazide, steroids, hypolipidemic drugs, oral contraceptives, anticoagulants)
The data obtained were analysed using SPSS software 21.0 software.
Results were expressed in frequencies and percentages.
36
OBSERVATIONS AND RESULTS
TABLE 1- AGE DISTRIBUTION
AGE IN YEARS NO OF PATIENTS PERCENTAGE
< 30 13 6%
31-40 24 12%
41-50 54 27%
51-60 60 30%
> 60 49 25%
CHART 1- AGE DISTRIBUTION
6%
12%
27%
30%
25%
AGE DISTRIBUTION
< 30 31-40 41-50 51-60
> 60
37
TABLE 2- SEX DISTRIBUTION
SEX NO OF PATIENTS PERCENTAGE
MALE 131 65%
FEMALE 69 35%
CHART 2- SEX DISTRIBUTION
65%
35%
SEX DISTRIBUTION
MALE FEMALE
38
TABLE 3- LIPID PROFILE
LIPID PROFILE ABNORMAL NORMAL
TOTAL CHOLESTEROL 64 136
TRIGLYCERIDES 133 67
HDL 91 109
LDL 116 84
CHART 3- LIPID PROFILE
64
133
91
116 136
67
109
84
0 20 40 60 80 100 120 140 160
TOTAL CHOLESTEROL TRIGLYCERIDES HDL LDL
LIPID PROFILE
ABNORMAL NORMAL
39
TABLE 4- MEAN CHOLESTEROL VALUE BASED ON SEX
SEX
TOTAL CHOLESTEROL
MEAN SD
MALE 155.89 46.59
FEMALE 162.3 46.67
P VALUE - 0.356 UNPAIRED T TEST NON SIGNIFICANT
CHART 4- MEAN CHOLESTEROL VALUE BASED ON SEX
155.89 162.3
M A L E F E M A L E
SEX VS TC
40
TABLE 5- MEAN TRIGLYCERIDE VALUE BASED ON SEX
SEX
TRIGLYCERIDES
MEAN SD
MALE 173.89 99.79
FEMALE 162.3 91.24
P VALUE - 0.854 UNPAIRED T TEST NON SIGNIFICANT
CHART 5- MEAN TRIGLYCERIDE VALUE BASED ON SEX
173.89
162.3
156 158 160 162 164 166 168 170 172 174 176
MALE FEMALE
SEX VS TGL
41
TABLE 6- MEAN HIGH DENSITY LIPOPROTEIN CHOLESTEROL BASED ON SEX
SEX
HDL
MEAN SD
MALE 44.69 15.66
FEMALE 49.99 14.01
P VALUE - 0.019 UNPAIRED T TEST
SIGNIFICANT
CHART 6- MEAN HIGH DENSITY LIPOPROTEIN CHOLESTEROL BASED ON SEX
44.69
49.99
42 43 44 45 46 47 48 49 50 51
MALE FEMALE
SEX VS HDL
42
TABLE 7 - MEAN LOW DENSITY LIPOPROTEIN CHOLESTEROL BASED ON SEX
SEX
LDL
MEAN SD
MALE 129.54 18.35
FEMALE 132.92 17.06
P VALUE - 0.198 UNPAIRED T TEST NON SIGNIFICANT
CHART 7 - MEAN LOW DENSITY LIPOPROTEIN CHOLESTEROL BASED ON SEX
127 128 129 130 131 132 133
MALE FEMALE
129.54
132.92
SEX VS LDL
43
TABLE 8- DISTRIBUTION BASED ON BODY WEIGHT
BODY MASS INDEX NO OF PATIENTS PERCENTAGE
UNDERWEIGHT 2 1.00%
NORMAL 122 61%
OVERWEIGHT AND OBESE 76 38%
CHART 8- DISTRIBUTION BASED ON BODY WEIGHT
1%
61%
38%
BODY MASS INDEX
UNDERWEIGHT NORMAL OVERWEIGHT
44
TABLE 9- COMPARISON BETWEEN BMI AND CHOLESTEROL
BMI
TOTAL CHOLESTEROL
MEAN SD
UNDERWEIGHT 158 3.74
NORMAL 158.97 48.26
OVERWEIGHT 156.71 44.2
P VALUE - 0.947 UNPAIRED T TEST NON SIGNIFICANT
CHART 9- COMPARISON BETWEEN BMI AND CHOLESTEROL
158
158.97
156.71
155.5 156 156.5 157 157.5 158 158.5 159 159.5
UNDERWEIGHT NORMAL OVERWEIGHT
BMI VS TC
45
TABLE 10- COMPRISON BETWEEN BMI AND TRIGLYCERIDE
BMI
TRIGLYCERIDES
MEAN SD
UNDERWEIGHT 80.5 33.23
NORMAL 168.31 88.39
OVERWEIGHT 182.88 18.75
P VALUE - 0.023 UNPAIRED T TEST
SIGNIFICANT
CHART 10- COMPARISON BETWEEN BMI AND TRIGLYCERIDE
80.5 168.31 182.88
U N D E R W E I G H T N O R M A L O V E R W E I G H T
BMI VS TGL
46
TABLE 11- COMPARISON BETWEEN BMI AND HDL-C
BMI
HDL
MEAN SD
UNDERWEIGHT 50 2.82
NORMAL 46.2 13.99
OVERWEIGHT 46.92 12.4
P VALUE UNPAIRED T TEST NON SIGNIFICANT
CHART 11- COMPARISON BETWEEN BMI AND HDL-C
50 46.2 46.92
U N D E R W E I G H T N O R M A L O V E R W E I G H T
BMI VS HDL
47
TABLE 12- COMPARISON BETWEEN BMI AND LDL-C
BMI
LDL
MEAN SD
UNDERWEIGHT 148 19.79
NORMAL 131.75 18.5
OVERWEIGHT 128.63 16.73
P VALUE - 0.194 UNPAIRED T TEST NON SIGNIFICANT
CHART 12- COMPARISON BETWEEN BMI AND LDL-C
148
131.75
128.63
115 120 125 130 135 140 145 150
UNDERWEIGHT NORMAL OVERWEIGHT
BMI VS LDL
48
TABLE 13- DISTRIBUTION OF WAIST CIRCUMFERENCE WAIST CIRCUMFERENCE NO OF PATIENTS PERCENTAGE
HIGH 4 2.00%
NORMAL 196 98%
CHART 13- DISTRIBUTION OF WAIST CIRCUMFERENCE
2%
98%
WAIST CIRCUMFERENCE
HIGH NORMAL
49
TABLE 14- COMPARISON BETWEEN WC AND CHOLESTEROL
WAIST CIRCUMFERENCE
TOTAL CHOLESTEROL
MEAN SD
HIGH 182.75 44.04
NORMAL 157.6 46.26
P VALUE - 0.028 UNPAIRED T TEST
SIGNIFICANT
CHART 14- COMPARISON BETWEEN WAIST CIRCUMFERENCE AND CHOLESTEROL
182.75 157.6
H I G H N O R M A L
WC VS TC
50
TABLE 15- COMPARISON BETWEEN WC AND TRIGLYCERIDES
WAIST CIRCUMFERENCE
TRIGLYCERIDES
MEAN SD
HIGH 187.8 123.02
NORMAL 172.67 96.45
P VALUE - 0.162 UNPAIRED T TEST NON SIGNIFICANT
CHART 15- COMPARISON BETWEEN WC AND TRIGLYCERIDES
165 170 175 180 185 190
HIGH NORMAL
187.8
172.67
WC VS TGL
51
TABLE 16- COMPARISON BETWEEN WC AND HDL
WAIST CIRCUMFERENCE
HDL
MEAN SD
HIGH 60.75 8.34
NORMAL 46.22 15.26
P VALUE - 0.05 UNPAIRED T TEST
SIGNIFICANT
CHART 16- COMPARISON BETWEEN WC AND HDL
60.75 46.22
H I G H N O R M A L
WC VS HDL
52
TABLE 17- COMPARISON BETWEEN WC AND LDL
WAIST CIRCUMFERENCE
LDL
MEAN SD
HIGH 130.5 22.95
NORMAL 130.7 17.91
P VALUE - 0.979 UNPAIRED T TEST NON SIGNIFICANT
CHART 17- COMPARISON BETWEEN WC AND LDL
130.5 130.7
H I G H N O R M A L
WC VS LDL
53
TABLE 18- DISTRIBUTION OF WAIST HIP RATIO WAIST HIP RATIO NO OF PATIENTS PERCENTAGE
HIGH 27 13.00%
NORMAL 173 87%
CHART 18- DISTRIBUTION OF WAIST-HIP-RATIO
13%
87%
WAIST HIP RATIO
HIGH NORMAL
54
TABLE 19- COMPARISON OF WHR AND CHOLESTEROL
WHR
TOTAL CHOLESTEROL
MEAN SD
HIGH 174.81 51.95
NORMAL 155.48 45.82
P VALUE - 0.045 UNPAIRED T TEST
SIGNIFICANT
CHART 19- COMPARISON OF WHR AND CHOLESTEROL
174.81 155.48
H I G H N O R M A L
WHR VS TC
55
TABLE 20- COMPARISON OF WHR AND TRIGLYCERIDE
WHR
TRIGLYCERIDES
MEAN SD
HIGH 186.7 113.59
NORMAL 170.83 93.9
P VALUE - 0.429 UNPAIRED T TEST NON SIGNIFICANT
CHART 20- COMPARISON OF WHR AND TRIGLYCERIDE
186.7
170.83
160 165 170 175 180 185 190
HIGH NORMAL
WHR VS TGL
56
TABLE 21- COMPARISON OF WHR AND HDL
WHR HDL
MEAN SD
HIGH 49.22 15.69
NORMAL 46.69 15.21
P VALUE - 0.324 UNPAIRED T TEST NON SIGNIFICANT
CHART 21- COMPARISON OF WHR AND HDL
45 45.5 46 46.5 47 47.5 48 48.5 49 49.5
HIGH NORMAL
49.22
46.69
WHR VS HDL
57
TABLE 22- COMPARISON OF WHR AND LDL
WHR LDL
MEAN SD
HIGH 132.81 15.97
NORMAL 130.4 18.26
P VALUE - 0.518 UNPAIRED T TEST NON SIGNIFICANT
CHART 22- COMPARISON OF WHR AND LDL
132.81 130.4
H I G H N O R M A L
WHR VS LDL
58
TABLE 23- COMPARISON BETWEEN FASTING BLOOD SUGAR AND SBP
SBP
FBS
MEAN SD
HIGH 171.15 42.36
NORMAL 185.45 42.72
P VALUE - 0.018 UNPAIRED T TEST
SIGNIFICANT
CHART 23- COMPARISON BETWEEN FASTING BLOOD SUGAR AND SBP
171.15
185.45
160 165 170 175 180 185 190
HIGH NORMAL
