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To determine whether the combination of obesity and hypertension results in additive defects in oxidative and nonoxidative glucose metabolism and the association of these changes with altered hemodynamic actions of insulin, we studied 11 abdominally obese hypertensive, 6 abdominally obese normotensive, and 7 lean normotensive nondiabetic subjects. Endogenous glucose production and glucose metabolized were calculated from a euglycemic clamp at 72 and 287 pmol insulin/m2 per minute. Glucose metabolized divided by insulin was lower at 72 pmol/m2 per minute in both obese groups than in lean normotensive subjects, at 148 +/- 14, 144 +/- 33, and 373 +/- 69 (mumol/m2 per minute)/(pmol/L), respectively (P < .01). Similar results were obtained during the higher insulin dose. Nonoxidative and oxidative glucose disposals by indirect calorimetry were lower in both abdominally obese groups (P < .05). Hepatic glucose production was completely suppressed in lean subjects at the lower insulin dose and in all three groups at the higher insulin dose. Hemodynamic responses during the clamp were not significantly different among the three groups. Abdominal obesity is associated with defects in insulin-regulated oxidative and nonoxidative glucose disposal as well as in insulin suppression of hepatic glucose production. Mild hypertension does not exacerbate these defects. Whereas the global impairment in glucose metabolism suggests the presence of an early defect or defects, including reduced tissue perfusion, systemic and regional hemodynamic responses to insulin were not altered. These findings do not support a direct role for insulin resistance in the pathogenesis of the hypertension associated with abdominal obesity.
Hypertension 1995 Jul
PMID:Glucose metabolism in abdominally obese hypertensive and normotensive subjects. 760 22

Central obesity in association with insulin resistance is a strong predictor of coronary artery disease (CAD) in South Asians; however the prevalence of central obesity and insulin resistance in Indians are unknown. Anthropometric measurements, dietary intakes, physical activity and prevalence of risk factors and CAD were obtained in 152 adults between 26-65 years of age (80 males, 72 females) selected by random sampling from urban population of Moradabad. The overall prevalence of central obesity was 539 per 1000 adults including 56.2% in males and 51.3% in females. The prevalence of glucose intolerance, diabetes mellitus, hypertension, hypertriglyceridemia and CAD were significantly higher in the higher quintiles of WHR above 0.88 compared to lower quintiles. Fasting and postprandial glucose, plasma insulin and triglycerides as well s total cholesterol and blood pressure were significantly higher in each of the upper quintile of WHR with increase in WHR compared to lowest quintile of WHR below 0.81. These findings indicate the existence of a modest degree of insulin resistance with a modest tendency to central obesity in the urban population of North India. The prevalence of CAD was significantly (p < 0.01) higher among subjects with central obesity than in non-obese subjects (21.5 vs 3.2%). Underlying these findings, the prevalence of central obesity was significantly greater among sedentary and mild activity group compared to moderate and heavy activity group and per day energy expenditure during activity in the upper quintiles with WHR > 0.88 was significantly less compared to energy expenditure in lower quintiles of WHR. Similarly dietary fat intake in the upper quintiles of WHR was also significantly higher than in the lower quintiles of WHR. These findings suggest that populations with higher prevalence of central obesity and CAD may be benefited with an aim to decrease central obesity.
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PMID:Epidemiologic study of central obesity, insulin resistance and associated disturbances in the urban population of North India. 767 61

Unlike classical microvascular complications, large-vessel atherosclerosis can precede the development of diabetes, suggesting that rather than atherosclerosis being a complication of diabetes, both conditions have common genetic and environmental antecedents, i.e., they spring from a "common soil." It is now known that adverse environmental conditions, perhaps related to less-than-optimal nutrition, in fetal and early life are associated with an enhanced risk of both diabetes and cardiovascular disease many decades later. These same adverse environmental conditions are also associated with the development in adult life of abdominal obesity and the insulin-resistance syndrome (IRS). The IRS consists of glucose intolerance, hyperinsulinemia, dyslipidemia (high triglyceride and low high-density lipoprotein [HDL] cholesterol levels), and hypertension. Although the mechanism underlying this cluster is controversial, the statistical association is well established. All of the elements of the IRS have been documented as risk factors for type II diabetes. Some, but not all, of these elements are also cardiovascular disease risk factors, in particular, hypertension and low HDL cholesterol. Other factors associated with the IRS that may enhance cardiovascular disease risk are plasminogen activator inhibitor 1 and small, dense low-density lipoprotein particles. Whether insulin itself is a risk factor remains controversial, but recent epidemiological evidence has been mostly negative. This question has marked clinical relevance because if the IRS enhances cardiovascular disease risk by virtue of its concomitant factors and not the hyperinsulinemia per se, this would tend to alleviate concerns that intensive insulin management of type II diabetic subjects could enhance the risk of large-vessel atherosclerosis. Clinical trials are urgently needed to settle this point.
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PMID:Diabetes and cardiovascular disease. The "common soil" hypothesis. 769 2

The relationship between overweight and cardiovascular disease was a matter of debate for many years. Recent studies have demonstrated that obesity defined as body mass index of 30 kg/m2 or higher is associated with an exponential increase of cardiovascular complications. This effect is largely mediated by the induction of established risk factors such as dyslipidemia, hypertension and type 2 diabetes mellitus. Recently, there is growing evidence that the occurrence of most complications of obesity depends not only on the degree of overweight but also on the pattern of body fat distribution. Many data suggest that the anatomical localization of body fat is more important for the risk of developing complications than the adipose tissue mass per se. An abdominal, upper-body type of fat distribution, which can be easily determined by the measurement of waist and hip circumferences (waist/hip ratio = WHR), is also a confirmed risk factor for metabolic disturbances, hypertension and atherosclerosis, independent of body weight. However, the clinical appearance of these disturbances is frequently associated with the development of obesity. This network of metabolic disorders and their vascular complications is termed "metabolic syndrome" or "syndrome X" (Table 2). Abdominal obesity is now known to be closely associated with the metabolic syndrome and is regarded to represent its readily recognizable phenotypic feature. The components of the metabolic syndrome are characterized by varying forms and degrees of insulin resistance. It is assumed that insulin resistance, defined as diminished biological response to the action of insulin, represents the primary defect or at least the common pathogenetic link between these disturbances.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Abdominal obesity and coronary heart disease. Pathophysiology and clinical significance]. 771 76

The metabolic syndrome usually goes along with abdominal obesity: diabetes type II, hypertension, dyslipidemia, and gout are often associated. The common characteristic is the resistance to insulin action. Reasons for the metabolic syndrome are--besides a genetic determination--overnutrition, physical inactivity, and alcohol consumption. Therefore, a causal therapy aims at the elimination of these factors. Consequently, the non-pharmacological therapy of the metabolic syndrome should be emphasized. The most important treatment is the reduction of body weight in the presence of obesity which is relevant for almost 90% of the patients. Body weight can rapidly be diminished by hypocaloric diets. Both, conventional reducing diets or formula diets may be used for weight reduction. Total fasting should not be performed for several reasons. For minor weight reduction or weight maintenance following a period of rapid weight loss with a hypocaloric diet, increased physical activity also lowers weight or prevents relapsing. Aims of therapeutical procedures are the elimination or amelioration of insulin resistance and subsequently the diseases of the metabolic syndrome. Both methods, reducing diet and physical training, act on various factors related to insulin resistance. For example, hypocaloric diets activate thyroxine kinase of the insulin receptor and reduce glucose and insulin in plasma. Physical training reduces not only insulin and glucose in plasma but also free fatty acids in addition and increases capillary density in skeletal muscle. Using the glucose clamp technique, diets and training are equally effective in improving glucose metabolism. Compared to these non-pharmacological methods drugs are less convincing. Since the non-pharmacological treatment implies behavioral changes with regard to nutrition, physical activity and alcohol consumption, simple instructions are not sufficient. Usually long-lasting changes in life style are necessary in order to achieve health improvement. Therefore, health care programs on individual or social basis are required in order to improve nutrition and increase physical activity. However, long-acting effects are difficult to achieve in adults; more promising is the prevention of insulin resistance.
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PMID:[Non-pharmacological therapy of metabolic syndrome]. 771 78

Type IIB muscle fibres are among the most insulin-insensitive muscle fibres and are not adapted to oxidation of fat during muscle work. The first characteristic of this type of muscle fibre most probably reflects or contributes to further development of insulin resistance contribute to further perpetuation of obesity and to the channeling of excess free fatty acids to the liver followed by secondary deterioration of its function. The impaired functioning of the liver is epitomized, among other changes, by impairment of insulin extraction. The increasing hyperinsulinaemia is followed by inhibition of synthesis of specific proteins such as carrier proteins for transporting testosterone (sex hormone binding globulin, SHBG). This results in an increased free testosterone concentration which induces androgenization in women and may further increase insulin insensitivity in abdominal obesity in women. The poor capillarization and changed muscle morphology in spite of great interindividual variety is observed in several pathological conditions characterised by insulin sensitivity (stroke, PCO, hypertension, diabetes, obesity). It is suggested that, in addition to the previous concept of the main role of intraabdominal adipose tissue, even muscles and liver are also important organs contributing to the pathogenesis and development of the metabolic syndrome.
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PMID:Role of muscle morphology in the development of insulin resistance and metabolic syndrome. 783 Dec 32

To determine the prevalence of coronary risk factors and coronary heart disease (CHD) in rural Rajasthan, 1150 randomly selected individuals in a cluster of villages in central Rajasthan have been studied. These included 805 men and 345 women. The prevalence of various coronary risk factors in the whole group were: Smoking 488 (42.4%); Diabetes (history): 5(0.4%); Alcohol intake: 146 (12.7%); Sedentary lifestyle: 797 (69.3%); Stressful life events: 48 (4.2%); Hypertension (BP > or = 140/90) 152 (13.2%); obesity (BMI > or = 27 Kg/M2): 194 (10.9%); and Truncal obesity (waist:hip > or = 0.93): 20.8%. The overall prevalence of CHD was 46.1/1000. Patients with CHD had a higher prevalence of male sex (67.9 vs 51.5%); educated persons (30.2 vs 28.8%); businessmen (13.2 vs 10.2%); smoking (47.2 vs 40.5%); sedentary lifestyle (75.5 vs 62.3%); stressful life events (7.5 vs 4.8%); and hypertension (26.4 vs 14.8%). On the other hand, persons without CHD had higher prevalence of alcohol intake (10.8 vs 7.5%); regular prayers (23.1 vs 22.6%); physically active lifestyle (37.7 vs 24.5%); obesity (13.6 vs 6.9%), and truncal obesity (21.0 vs 20.0%). The following risk factors emerged significant on statistical analysis (Odds ratio, 95% confidence intervals): male sex (1.99, 1.04 to 3.7); hypertension (2.04, 1.01 to 4.09); male smokers (1.80, 1.28 to 4.09); and sedentary lifestyle (1.86, 1.01 to 3.59). This study shows a low prevalence of CHD in rural population which is however more than previously reported studies from India.
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PMID:Coronary heart disease and coronary risk factor prevalence in rural Rajasthan. 783 42

Numerous prospective epidemiological studies point out high mortality prevalence in diabetic subjects. Classical risk factors, especially arterial hypertension and hypertriglyceridaemia, are abnormally associated with diabetes mellitus. However, they don't account for overall surmortality in this disease. Additional markers of cardiovascular risk appeared as albuminuria, abdominal obesity, and the couple insulinoresistance/hyperinsulinism. Physiopathological intrinsic mechanisms inherent to macroangiopathy are multiple and intricate (hemostatic disorders, endothelial impairments, oxidative stress, quantitative and qualitative lipoproteins abnormalities, part of hyperinsulinism and growth factors). Strict normoglycaemia and exacting control of all other risk factors is essential. Use of other therapeutic agents as antioxidants and antiagregants, is discussed.
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PMID:[Diabetes mellitus and atherosclerosis. Physiopathology of diabetic macroangiopathy]. 787 Dec 68

Truncal obesity has been identified as a risk factor for coronary heart disease (CHD). We studied 399 males for waist hip ratio (WHR) measurement during a comprehensive cardiovascular survey in a rural population of Rajasthan. The WHR measurements were correlated with coronary risk factors and CHD prevalence. The mean WHR in the study population was 0.88 +/- 0.11. The median value was 0.88 with a range of 0.49 to 1.59. Multiple regression analysis showed a significant positive relationship of WHR with height (b = 0.77, p = 0.02), weight (b = 1.48, p = 0.02), body mass index (b = 1.44, p = 0.01) and systolic (b = 0.12, p = 0.05) and diastolic blood pressure (b = 0.13, p = 0.03) but not with age, educational level, total LDL- or HDL- cholesterol and triglycerides. The median value of 0.88 was taken to classify the study population for risk factor analysis. There were 200 males with WHR < or = 0.88 (Group A) and 199 males with WHR > or = 0.88 (Group B). Group B men had significantly higher body-weight and body-mass index and there was a trend towards lower serum HDL cholesterol and higher triglyceride levels in this group which was not statistically significant. The prevalence of hypertension was similar in the two groups. The prevalence of coronary heart disease was significantly higher in Group B.
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PMID:Correlation of waist-hip ratio with coronary heart disease and risk factor prevalence in a rural male population. 787

Because of its association with a constellation of cardiovascular risk factors, insulin resistance has recently emerged as a major clinical disorder. There is therefore an increasing need to accurately assess insulin sensitivity in clinical and epidemiologic studies. The merits of various techniques for measuring insulin action are briefly reviewed. Essential hypertension and insulin resistance appear to be tightly linked; however, the mechanism or mechanisms accounting for this association are not known. Central or intra-abdominal obesity is a particularly strong risk factor for the development of hypertension. The weight of the evidence suggests that hyperinsulinemia per se is not a potent instrumental factor in the development of hypertension. Mechanisms suggesting that insulin resistance independent of hyperinsulinemia may predispose to increased vascular tone are discussed. Conversely, the possibility that essential hypertension could engender insulin resistance is proposed. The link between insulin resistance and hypertension is likely to be complex and multifactorial.
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PMID:Pathogenesis and measurement of insulin resistance in hypertension. 788 89


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