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Asia Pacific J Clin Nutr (1994) 3, 33-39

Asia Pacific J Clin Nutr (1994) 3, 33-39

Body composition in the pathogenesis and management of diabetes: a Malaysian perspective

Ali Osman* MD, MPH, PhD and B.A.K. Khalid** MBBS, PhD, FRACP

*Department of Community Health, **Dean, Faculty of Medicine, 53000, Kuala Lumpur, Malaysia.

There is an increasing prevalence of diabetes mellitus around the world associated with rapid sociocultural development and changing lifestyles. Increased prevalence of obesity, with a higher consumption of animal products and lower consumption of fruits and vegetables, increases the risk of diabetes mellitus and other chronic degenerative diseases. Insulin-dependent diabetes (IDD) is caused by insulin deficiency, whereas the main feature of non-insulin-dependent diabetes (NIDD) which accounts for more than 90% of diabetics, is hyperinsulinemia and insulin resistance, which may eventually lead to actual insulin deficiency. Hyperinsulinemia is undesirable because it increases the risk of developing vascular disease. In Malaysia, the prevalence of NIDD in some communities now exceeds 5%, and of impaired glucose tolerance 10%. Along with these increases in prevalence of hyperglycemia are increases in prevalence of overweight (BMI>25) and almost certainly abdominal fatness. In terms of management, nutrition is given priority. Insulin and hypoglycemic drugs (sulphonylureas or biguanides), where required, may adversely affect body composition if overused. Newer therapeutic strategies require greater attention to the underlying problem in NIDD of abdominal fatness by attention to the relevant nutritional factors, physical activity and other lifestyle factors like cigarette smoking and alcohol. The greater impact of obesity and diabetes on Malaysian women as opposed to men also needs to be addressed.


Diabetes mellitus was described as early as 1600 BC as a disease with polyuria and insatiable thirst but the detailed description of the disease and its pathogenesis did not exist until the nineteenth century. This disease occurs in almost all populations; however, the prevalence varies depending on the population, its age structure, genetic background and lifestyle. High prevalences are found among the Pima Indians in North America, Nauruans, Indians and Australian Aborigines1 and low prevalence among the Melanesians in Solomon Islands. Part of the heterogeneity between populations is probably accounted for by body composition, in turn dependent on diet, physical activity and substance abuse, over and above genetic background2. The present report draws on recent observations of increasing prevalences among Malaysians.

Genetic vs environmental factors

Community-based studies from Malaysia show that the prevalence of diabetes is highest among urban Malays and is lower whe 1000 re the socio-economic development is less (Table 1). However, urban Malays have lower prevalences of impaired glucose tolerance (IGT) compared to their rural counterparts. On the other hand, the prevalence of diabetes mellitus and IGT among Malaysian aborigines (Orang Asli) is very low in all locations. Certain genetic factors for the moment probably protect the Orang Asli from the disease, whereas environmental influences have already increased the prevalence among genetically susceptible Malays. Community comparisons of fasting, 2 hour post-glucose load and Hb A1 values support an environmental influence on diabetes occurrence (Table 2).

Table 1. Crude and adjusted prevalence rates of diabetes mellitus and IGT (per cent)3.

  Diabetes mellitus IGT
Stages of development crude rate age-adjusted* 95% I** crude rate age-adjusted* 95% I**
Remote rural
Lanai (n=110) (ABO) 0.0 0.0 -- 3.3 4.9 0.6-17.6
Ulu Sungai (n=136) (MAL) 2.8 2.7 0.6-8.1 14.8 15.0 8.6-24.0
Betau (n=136) (ABO) 1.3 1.7 0.1-9.5 10.7 12.6 5.9-25.2
Koyan (n=132) (MAL) 6.7 7.4 3.0-15.5 10.5 8.5 4.3-15.3
Lanjan (n=75) (ABO) 0.0 0.0 - 0.0 0.0 --
Kg. Kerinci (n=92) 8.2 7.7 2.9-16.9 9.6 7.6 3.0-16.0

ABO = Orang Asli. MAL = Malays. * Five-year age-specific rates (30-64 years) were calculated and standardization was performed using the direct method against the standard population of Segi. ** 95% confidence interval based on Poisson distribution.

Table 2. Blood glucose and HbA1 by social development3.

Stages of development Fasting blood glucose (mM) 2 hours post glucose load (mM) HbA1 (%)
Remote rural      
Lanai Aborigines settlement      
N 111 98 87
means sd 5.0 1.0* 5.1 1.7* 4.5 0.8*
Ulu Sungai Malay village      
n 152 142 100
means sd 5.4 1.7 6.1 3.2 5.5 1.7
Betau Aborigines settlement      
n 136 115 74
means sd 4.8 0.5** 5.3 1.3** 4.4 0.5**
Sungai Koyan Malays resettlement scheme      
n 114 109 78
means sd 5.1 0.8 6.3 2.5 5.6 1.7
Lanjan Abongines village      
n 73 70 73
means sd 5.1 0.8 5.0 1.2*** 4.8 0.6***
Kerinci Malays village      
n 90 81 89
means sd 5.3 1.9 6.1 3.8 5.8 1.8

Values are means sd. *P<0.05 vs remote rural Malays. **P<0.05 vs rural Malays. ***P<0.05 vs urban Malays.

Nutrition and diabetes mellitus

Various epidemiological studies have shown that a high consumption of refined carbohydrates and fats, low intake of dietary fibre, together with obesity and on inactive lifestyle contribute to the development of non-insulin-dependent diabetes (NIDD)4-6. Increased per capita energy consumption per day, especially of oils and fats, animal products and sugar, with a concomitant decline in the dietary energy from complex carbohydrates such as cereals and other plant products (pulses, nuts and oilseeds, fruits and vegetables) are associated with a high risk of developing NIDD. Ingestion of carbohydrates has not been shown to increase the risk of diabetes except by virtue of contributing to excessive weight gain7, although there is interest in partial substitution of carbohydrate with monounsaturated oils, as in the Mediterranean diet, as a way of minimizing hyperglycemial9a.

Epidemiology of obesity and diabetes mellitus

Overweight and obesity are important determinants of NIDD whether in the city or in the village. Data available from epidemiologic studies and surveys in the USA indicates that 24% of American women and 22% of men are obese, by criteria of relative body weight (>120%) or BMI >27.5 kg.m-2. In general, obesity is common among women from lower socio-economic groups8 and with lower education. The prevalence of overweight and obesity (BMI 25) in developing countries such as Malaysia is on an upward trend (Table 3), for urban subjects about 25-30% and rural subjects 5-15%. The prevalence of diabetes among overweight Malaysian subjects BMI 25 was 7.3% (9/123) compared to 1.6% (9/560) with BMI <253. Malay females have a six-fold risk of developing diabetes compared to males, and they also have a greater prevalence of overweight and obesity.

Table 3. Prevalence of overweight among Malaysians as indicated by BMI4.

Age groups (years) Population Number Gender Criteria of overweight (BMI) (kg/m2) Prevalence of overweight
  rural Malays 522 male 25.0 5%
18+ rural Malays 965 female 25.0 15%
25-34 Urban executives 146 male 25-30 26%
35-44 of mixed 209     29%
45-54 ethnicity 51     33%

Pathogenesis of diabetes mellitus

There is a complex interaction between genetic predisposition and environmental factors in the pathogenesis of diabetes. Diabetes is not a single disorder but a heterogenous syndrome with varying pathogenesis. There are broadly two different forms of the disease type I (insulin-dependent, IDD) and type II (non-insulin-dependent, NIDD)9. Approximately 90% of diabetics are type II. The differences in characteristics are shown in Table 4. The development of type I (IDD) diabetes is based on a chronic, progressive inflammation of the islet cells (insulinitis) due to the presence of antibodies against the cells. Hyperglycemia develops because of insulin deficiency of the B-cells. Environmental factors, possibly including diet are increasingly regarded as important in the pathogenesis. Type II diabetes (NIDD) is related to insulin resistance and defective or insufficient insulin receptors.

Table 4. Comparison between IDD and NIDD.

IDDM (type I) NIDDM (type II)
Prevalence approx 0.2%
Rapid onset of the disease*
Mostly in young age of <40
No frequency difference by sex
Nutritional status - thin
Environmental factors play important roles (viruses or chemicals)
Presence of islet-cell antibodies
Poor insulin production or total deficiency
Absolute insulin deficiency
Good insulin sensitivity
Ketosis prone
No response to sulphonylureas
Prevalence >3%
Slow onset
Generally onset after age of 40
More frequent in female
Normal or obese
Genetic factors plays important roles
ICA not present
Reduced insulin production or hyperinsulinemia
Insulin resistance or relative insulin deficiency
Poor insulin sensitivity
Ketosis resistant except during infection or stress
Good response to sulphonylureas

*Although the onset symptoms in IDD is abrupt, its revolution may involve an antecedent period of slowly developing autoimmune to the pancreatic B ceils.


Body composition and NIDD

The prevalence of overweight among people with NIDD is more than 80%; that of abdominal obesity may even be higher. Individuals who are 40% overweight have almost a seven times greater chance of having diabetes mellitus as individuals of normal weight (Figure 1). Diabetic morbidity also rises as body weight increases7. The predominant and most characteristic anatomic changes among obese individuals is the excessive accumulation of adipose tissue or increased body fat content in certain parts of the body. Determination of overfatness by skin fold thickness (SFT) and by BMI for total body fatness have become the most widely used means of assessing body fatness10. With SFT and truncal circumferences, distribution in body fatness can also be ascertained.

Fig 1. Incidence of diabetes and body weight (from Diabetes Source Book, 1969).

Many studies have shown that obesity as indicated by body mass index (BMI) is significantly associated with incidence or prevalence of diabetes11-13. Other nutritional indices such as mid-arm circumference (MAC) and triceps skin fold thickness (TSFT) subscapular and supralic skin folds (SSSF and SSISFT) also support the importance of obesity (in particular upper body obesity) in the development of diabetes. Upper body obesity not only predicts the prevalence of diabetes mellitus but also IGT (P<0.0001)3. Abdominal fat distribution in men and women also predicts certain risk factors of macrovascular disease, such as hypertriglyceridemia and hypertension. The mechanism by which abdominal fatness increases the risk for NIDD is not clear. Adipose tissue located in the abdomen is more sensitive to lipolytic stimuli than adipose tissue elsewhere51. The lipolytic products, glycerol and free fatty acid (FFA), are directly delivered to the liver in the splanchnic circulation and enhance gluconeogenesis and Very Low Density Lipoprotein-Triglyceride (VLDL-synthesis)5l; FFA also reduce peripheral glucose uptake50; hypertriglyceridemia increases7.

Fat distribution rather than total fat is a better predictor for NIDD. Upper body obesity is associated with high prevalence of NID 1000 D especially among women14-16. Biceps and subscapular skin fold thicknesses and waist-hip ratio are strongly associated with NIDD in many studies17-20.

Many obese patients have frank NIDD. They are not ketosis-prone and do not require exogenous insulin for blood glucose control. Many other obese patients have IGT. The prevalence in the community increases strikingly according to lifestyle changes leading to obesity. However, while obesity may be a very important risk factor for NIDD, it is and by itself, insufficient to produce this disease. A genetic susceptibility for NIDD may be necessary for obesity to induce clinical disease48-49. These are the processes which now require more intensive study in Malaysian communities.

Body composition and insulin resistance

One of the metabolic features of obesity especially upper body obesity is the existence of hyperglycemia in the face of hyperinsulinemia. This means insulin's ability to influence glucose metabolism is impaired, a condition referred to as insulin resistance. With abdominal fatness cells become less sensitive to insulin21 and insulin binding for receptors are reduced22.

Hyperinsulinemia in the presence of normal glucose tolerance is evident in young people in Pacific Ocean communities who have high susceptibility to NIDD. Subsequently, insulin resistance occurs which leads to secondary pancreatic b -cell exhaustion23-27. The exhaustion leading to an abnormality of insulin synthesis or secretion may be genetically determined. Both population surveys and prospective studies of prediabetic Pima Indians indicate that insulin resistance predates the onset of NIDD28,29. The 'thrifty genotype' in NIDD could contribute to insulin resistance in muscle. A selective insulin resistance in muscle would have the effect of blunting the hypoglycemia that occurs during fasting but would allow energy storage in fat and liver during feeding. Both of these features could allow hunter-gatherers to have survival advantages during periods of food shortage. However, in sedentary individuals allowed free access to food, these individuals become obese with secondary insulin resistance in fat and liver. Post-prandial hyperglycemia occurs would then lead to glucose toxicity with decreased insulin secretion from b -cells30.

Insulin resistance is recognized by diminished response to endogenous insulin (hyperinsulinemia with normal or elevated blood glucose concentration) or exogenous insulin (diabetes requiring very large doses of insulin). Such resistance may be due to changes in insulin receptors, post-receptor events, or both31. In obese individuals, the insulin resistance could result from impaired glucose uptake by peripheral tissues such as skeletal muscle and adipose tissue, impaired glucose uptake by the liver or increased hepatic glucose production. However, resistance to insulin action also occurs in lean individuals with NIDD. Thus it is considered that peripheral tissue insulin resistance is a characteristic of NIDD and obesity may not require to produce it27, unless subtle increases in abdominal visceral fat have not been recognized.

The number of receptors appears to be lower in obese patients7,13. One theory concerning the development of insulin resistance in obese NIDD postulates that repetitive postprandial hyperglycemia initially leads to a down regulation of insulin receptors, which then results in a compensatory increase in insulin secretion to prevent glucose intolerance. With more prolonged and greater hyperglycemia, postbinding defects in insu 1000 lin action then emerge. Decreases in the intracellular and plasma pools of glucose transporter may occur. Overt diabetes develops only in individuals whose pancreas is unable to meet the increased and sustained demand for insulin secretion24.

The cellular mechanism for insulin resistance in NIDD is still poorly understood. Early reports indicated the inconsistent relationship between insulin receptor binding and diabetes. However, more recent reports have found evidence for a postbinding defect in NIDD. Increased lipolysis in the glucose-fatty acid cycle is partly responsible for the post-insulin receptor resistance. Insulin resistance in NIDD is associated with increase in VLDL-TG and decrease in HDLC. However, whether insulin resistance causes increased VLDL or, conversely, whether elevations in VLDL impair insulin action, is yet to be determined33.

Hyperinsulinemia and associated insulin resistance with normal glucose tolerance and not impaired insulin secretion could be considered as an early phase in the development of NIDD24,34,35. Progression from normal to IGT is associated with a reduction in insulin sensitivity. However, glucose tolerance is mildly impaired with a further compensatory increase in insulin secretion. Syndrome X is the name given to the association of obesity, hypertension, hypertriglyceridemia, hyperuricemia and insulin resistance. It is conceivable that abdominal visceral obesity underlies most of the syndrome, and, in turn, genetic predisposition to it along with a fatty refined diet and physical inactivity. If this be the case, then greater attention to the increasing problem of NIDD, and underlying visceral obesity in Malaysia may have a useful impact on the Nation's health.

Management approach

The defective functioning of b -cells and insulin receptors are difficult to reverse. Therefore, treatment remains symptomatic correction of the metabolic defects. Exogenous insulin may not be effective due to a presence of insulin resistance. However, diet, oral hypoglycemic agents and exercise may be beneficial in obese NIDD23,36-38. Even so all treatment should be designed to suit individual patients in relation to ethnic groups' lifestyle, work schedule and education.

Dietary adjustment

Dietary adjustment to reduce weight is the choice for obese NIDD patients with insulin resistance. Weight loss results in an improvement in the metabolic aspects of the diabetic state of obese individuals with diabetes. In many patients, glucose, lipid, protein metabolism and insulin secretion and action are restored to normal. In others, weight loss improves the diabetic state but some metabolic derangements still persist32. The choice of the best diet may depend on the degree of obesity and the stage of progression of b -cell dysfunction39.

A reduced-energy regimen should consist of 50-55% carbohydrates, 15% protein and 30-35% fats (with a high percentage of polyunsaturated fats). Obese diabetics will benefit from weight reduction because reducing body weight actually reduces high glucose levels to normal (improved glucose tolerance)40. Many obese NIDD patients, in the earlier stages of diabetes, tolerate weight-maintenance high-carbohydrate, low-fat diets without deterioration of glucose tolerance. However, as their insulin reserve declines, high-carbohydrate diets may further raise glucose levels, so a lower carbohydrate diet seems preferable. However, in advanced NIDD with deficiency of insulin secretion, high-carbohydrate diets espe 1000 cially refined carbohydrates should be avoided39.

Diets which are high in carbohydrate and natural fiber content produce a lowering of blood glucose as well as a lowering of low-density lipoprotein cholestrol (LDLC) and triglycerides in patients with NIDD41. In such patients, glucose homeostasis improvement is due to increased insulin sensitivity. For obese patients with diabetes, increased fiber in the diet may also enhance satiety, thereby aiding in weight reduction. A study carried out in Oxford found that diets containing a very high proportion of beans (61% carbohydrate, 18% fat, 21% protein and 96.9 g of fibre per day) resulted in the whole of the glucose profile being lowered41. Delayed absorption can be achieved by delayed gastric emptying presumably by dietary fibres or by using 'swelling substances' and slow breakdown of carbohydrates7. Guar gum and pectin (soluble fibre) was found to delay the absorption and can be useful in NIDD.

The arteriosclerotic complications found in patients with diabetes have been attributed partly to elevated plasma lipid concentrations which are influenced by fat intake. Diets for patients with diabetes should therefore have reduced fat intake to correct the unfavourable lipid profile. Achievement of ideal weight, glycemic control, and when necessary, medical treatment of hyperlipidemias will retard the process of atherosclerosis. HMG Co-A reductase inhibitor (pravastatin), and other hypolipidemic agents such as gemfibrozil42, and bezafibrate reduce cardiovascular risk through the correction of dyslipidemias43.

Oral hypoglycemic drugs

Biguanies act to decrease absorption, inhibit gluconeogenesis, stimulate glucose conversion in muscle and fatty tissue and lower plasma lipid levels. Their action, therefore, is linked to the presence of endogenous or exogenous insulin and so they are particularly suitable for obese diabetics. The side effect of lactic acidosis is probably less with metformin than other biguanides7.

Sulphonylureas act by stimulating b -cells to release insulin (it depends upon the existence of b -cells) and helping glucose sensitize the cells. They are useful for NIDD which cannot be controlled by diet alone. In NIDD insulin is secreted after stimulation by glucose, but its secretion is delayed and at low peak. About 30% reduction of blood glucose level will be produced by using these drugs. Since sulphonylureas increase insulin secretion, they may be relatively contraindicated in obese people with diabetes and hyperinsulinism.

Physical activities

Physical activity improves physical fitness, increases energy expenditure, helps appetite regulation, favourably influences serum lipoproteins, lowers blood pressure and, importantly, decreases the risk of coronary artery disease. Physical training can increase insulin sensitivity42a. However, the long-term effects on blood glucose control with exercise alone are not proven. In NIDD, since the population is often obese and sedentary, exercise would be expected to have beneficial effects in promoting weight reduction and thereby improving glucose regulation44. Exercise alone may have a marked effect on the long-term metabolic abnormalities of NIDD. But exercise combined with diet that produces greater effects. Moreover, the weight loss produced by exercising is more easily maintained45,46.

Even through exercise programs may have beneficial effects for patients with diabet 1000 es in conjunction with diet or hypoglycemic agents, it is inappropriate to exercise all patients at the same level of intensity, duration and frequency47.

Weight reduction and sulphonylurea therapy can achieve a decrease in insulin resistance. Exercise and weight reduction in obese individuals are accompanied by increased insulin receptor binding and postbinding insulin actions.


The changing lifestyle, particularly in respect of fatty, refined diets and decreasing physical activity are likely to be contributing to visceral obesity, insulin resistance and related phenomena in Malaysia as elsewhere. Prevention and management of NIDD require greater research and understanding of these phenomena.


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Copyright 1994 [Asia Pacific Journal of Clinical Nutrition]. All rights reserved.
Please note: this article has been scanned and reformatted.
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