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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The production and catabolism of very low density lipoprotein triglycerides (VLDL-TG) were determined in 11 index patients with primary hypertriglyceridemia and in their 70 first-degree relatives. In the probands the mean value for VLDL-TG production rate was twice normal, and the mean fractional catabolic rate (FCR) was reduced to 50% from normal. A similar kinetic pattern was also observed in most hypertriglyceridemic relatives. In the normotriglyceridemic relatives the mean values of both kinetic parameters were comparable to those of controls. No kinetic differences were observed between families with familial hypertriglyceridemia, familial combined hyperlipidemia, or genetically unclassified hypertriglyceridemia (all diagnosed by lipoprotein phenotypes). Thus, no explanation for the phenotypic differences between the two forms of familial hyperlipoproteinemia was found in plasma VLDL-TG metabolism. When the families were grouped according to the VLDL-TG production rate of the proband, there was no significant difference between the VLDL-TG production rates of relatives of "overproducer" probands and relatives of the probands with normal VLDL-TG production rate. In contrast, relatives of low FCR probands had significantly lower mean FCR than the relatives of probands with a normal FCR. This difference in FCR was present both in hypertriglyceridemic and normotriglyceridemic relatives. These results suggest that the catabolism (lipolysis) of VLDL-TG is under genetic control, whereas the VLDL-TG production rate is mainly related to obesity. It is likely that hypertriglyceridemia often develops on the basis of VLDL overproduction in individuals who have a genetically low VLDL triglyceride removal (lipolytic) capacity.
Arteriosclerosis
PMID:Very low density lipoprotein triglyceride metabolism in relatives of hypertriglyceridemic probands. Evidence for genetic control of triglyceride removal. 337 19

Differences in body fat distribution between diabetics and nondiabetics have been recognized for several decades; diabetics have a more centralized or upper body fat pattern than nondiabetics. Recently, attention has focused on fat patterning and also on hyperinsulinemia as possible risk factors for cardiovascular disease, as well. The case for insulin as a cardiovascular risk factor is bolstered by theoretical considerations related to its possibly atherogenic effects on serum and arterial wall lipids. Empirical evidence for fat patterning and hyperinsulinemia as cardiovascular risk factors rests on six prospective epidemiologic studies, three on fat patterning and three on insulin. Although provocative, none of these studies can be regarded as definitive. In none was a dose-response effect demonstrated, and there are various inconsistencies within and across the studies. Moreover, in none of the studies were hyperinsulinemia and fat patterning evaluated simultaneously. This is of particular importance in view of the well-documented interrelationships between these two variables. For example, insulin resistance and hyperinsulinemia have been found to be greater in women with upper body obesity compared to women with lower body obesity of equivalent degree. Considerable progress has been made recently in understanding the mechanisms of the differential metabolic effects of these two types of obesity. The extent to which fat patterning and hyperinsulinemia are genetic or acquired has received relatively little attention. Further research on this question is warranted since elucidation of any environmental influences on these variables might suggest new clinical and public health control measures.
Arteriosclerosis
PMID:Body fat distribution and hyperinsulinemia as risk factors for diabetes and cardiovascular disease. 351 49

Obesity, hypertension, a high plasma level of glucose, and some lipid abnormalities (high plasma levels of cholesterol and triglycerides) often occur in the same individuals. Some authors have postulated that the elevated levels of plasma insulin in obese individuals may explain this association. To explore this hypothesis further, the relationships between body mass index, fasting plasma glucose and insulin, blood pressure, serum lipids, and apoproteins were investigated in a group of 2144 healthy middle-aged men. Analysis of the data show that the associations between body mass index and blood pressure or lipid variables are largely independent of plasma glucose and insulin. Plasma glucose is strongly related to blood pressure in nonobese subjects. Plasma insulin is not associated with blood pressure independently of body mass index and plasma glucose; however, the simultaneous elevation of body mass index, plasma glucose, and insulin is strongly associated with blood pressure. The results also confirm that plasma insulin is positively related to triglycerides and negatively related to high density lipoprotein cholesterol independently of plasma glucose and body mass index.
Arteriosclerosis
PMID:Body mass, blood pressure, glucose, and lipids. Does plasma insulin explain their relationships? 355 32

To investigate the reasons for the lack of sex differences in high density lipoproteins (HDL) observed in population studies of the Pima Indians, we selected 18 lean (9 men, 9 women, body mass index (BMI) less than 27) and 22 obese (12 men, 10 women, BMI greater than 27) Pima Indians for an inpatient study of HDL composition. We measured lipase activities and steroid hormone concentrations, both of which have previously been implicated in the control of HDL. The lean women had higher concentrations of HDL and HDL2 than did either the obese women or the lean or obese men. Lean women had significantly lower hepatic lipase activities and significantly higher concentrations of estradiol compared to obese women. Lean women also had different HDL2 composition, as indicated by the molar ratio of HDL2 cholesterol/A-I. Significant negative correlations between HDL and obesity measured by either BMI or percent body fat were observed in both sexes, but the slope of the relationship was steeper in women. Significant negative associations were observed between HDL or HDL2 concentrations and hepatic lipase in both sexes, and there were significant positive associations between HDL2 and plasma estradiol in women. The data suggest that obesity in this population has a stronger negative influence on HDL concentrations in women, possibly through changes in estradiol and hepatic lipase activities. Since there are so few lean women in the Pima population, the net result is that HDL levels in women in the population as a whole do not differ from those of men.
Arteriosclerosis
PMID:Lack of sex differences in high density lipoproteins in Pima Indians. Studies of obesity, lipase activities, and steroid hormones. 359 76

The degree of arteriosclerotic changes in the aorta and major vessels was inversely related to obesity (P less than 0.05) in an unselected series of 300 autopsies on subjects older than 50 years who had no hypertensive diseases. In addition, out of 11 subjects with very severe obesity, 9 showed no arteriosclerosis, and only 2 showed mild arteriosclerosis.
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PMID:The relationship between obesity and degree of arteriosclerosis. New autopsy findings. 360 80

Glycosylated hemoglobin levels reflect glucose homeostasis over the preceding months. Many investigators have reported levels of glycosylated hemoglobin in diabetics and have noted a strong correlation of these levels with lipids and lipoproteins, but not with HDL cholesterol. We report here the first population-based study of the predominant fraction of glycosylated hemoglobin, HbA1, and its correlates in nondiabetics. In 558 euglycemic adults (fasting plasma glucose less than 140 mg/dl) aged 40 to 79 years who had no history of diabetes, HbA1 was normally distributed, was unrelated to age, and was correlated with fasting plasma glucose in men and women and with obesity in women. After adjusting for age and obesity, HbA1 was significantly correlated with total plasma cholesterol and LDL cholesterol in both sexes and with total plasma triglyceride and VLDL cholesterol in men. HDL cholesterol was not significantly associated with HbA1 in men or women. These associations are similar, although weaker, than those reported in most studies of diabetics. The finding that the association of glycosylated hemoglobin with lipids and lipoproteins extends throughout the normal range of blood sugar suggests that this association may be relevant to both the excess risk of ischemic heart disease in diabetics and in nondiabetics with higher levels of fasting plasma glucose.
Arteriosclerosis
PMID:Population-based study of glycosylated hemoglobin, lipids, and lipoproteins in nondiabetic adults. 381 76

Prevalence of diabetes and increasing incidence mainly concern the type II diabetes, the etiopathogenesis of which is finally still unclarified. While the behaviour of the insulin secretion of type II diabetes is clarified as far as possible, research of the last years concentrates to disturbances of the insulin binding at the receptor, of the insulin efficiency after receptor binding as well as to the complicated interrelations between insulin secretion and peripheral effectiveness. On the one hand, metabolic sequels of malnutrition and obesity as well as decreasing muscle activity and muscle mass, on the other hand the genetic disposition plays an important role. Recently, insights into disturbed intracellular biochemical courses could be obtained and newer approaches for therapy could be found out. Significant could be the separation into perhaps still reversible findings in the manifestation of the irreversible late findings at the level of postreceptors after longer course of diabetes at least for the type IIb (adipose type). The diversity of etiopathogenetic factors demands substandardizations which would give only beginnings for prevention and optimized differential therapy. It cannot be denied that type II diabetes and arteriosclerosis partly have common genetic and exogenic causes.
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PMID:[Type 2 diabetes--etiopathogenetic aspects]. 391 10

Recent data suggest that the protection against ischemic heart disease afforded by high density lipoprotein (HDL) cholesterol (C) may be concentrated in the HDL2 subfraction. To examine the behavioral correlates of the HDL subfractions, we recalled 33 men and 17 women of a random sample from the Pacific Northwest Bell Telephone Company Health Survey. Adiposity and very low density lipoprotein (VLDL) triglyceride were negatively correlated with HDL2C. Smoking was not correlated with HDL2C, but was negatively correlated with HDL3C (men, rs = -0.635, p = 0.001; women, rs = -0.534, p = 0.014); this relationship was independent of alcohol consumption, adiposity, and VLDL triglyceride. Alcohol consumption was also more strongly related to HDL3C (men, rs = 0.248, p = 0.082; women, rs = 0.586, p = 0.007). Lecithin cholesterol acyltransferase (LCAT) mass was negatively related with HDL2C, but was positively correlated with HDL3C and apolipoprotein A-II. Smoking was negatively correlated with LCAT mass. Since it is believed that HDL3C is not associated with the risk of ischemic heart disease and since both smoking and alcohol consumption may mainly affect HDL3C, the current study suggests that the increase in risk of ischemic heart disease with smoking and the possible decrease with alcohol consumption may be mediated through mechanisms other than their effects on HDLC.
Arteriosclerosis
PMID:Epidemiological correlates of high density lipoprotein subfractions, apolipoproteins A-I, A-II, and D, and lecithin cholesterol acyltransferase. Effects of smoking, alcohol, and adiposity. 391 1

Lipids and lipoproteins were measured in 139 men and 145 women who were noninsulin-dependent diabetics (NIDDs) aged 45 to 64 years. Of these, 27 men and 16 women had had a previous definite myocardial infarction (MI). The NIDDs with MI (MI+) showed lower values of HDL and HDL2 cholesterol concentrations than NIDDs without previous MI (MI-) or NIDDS without any symptoms or electrocardiographic signs of coronary heart disease (CHD-). The inverse relationship between HDL, HDL2, and CHD was evident in both sexes, but it was particularly strong among male NIDDs. The difference in HDL and HDL2 cholesterol concentrations between the MI+ and MI- groups or between the MI+ and CHD- groups persisted after adjustment by analysis of covariance for the effect of physical activity, alcohol intake, obesity, duration of diabetes, and glycemic control. It is concluded that in a cross-sectional study, even among NIDDs with generally low HDL and HDL2 cholesterol concentrations, the presence of CHD is associated with a further depression of HDL and HDL2 cholesterol levels. Prospective studies are needed, however, to confirm that the association is predictive and not a consequence of CHD.
Arteriosclerosis
PMID:Association of low HDL and HDL2 cholesterol with coronary heart disease in noninsulin-dependent diabetics. 407 98

Correlation analyses between serum ascorbic acid and several risk factors of cerebro- and cardio-vascular diseases were performed on apparently healthy adults (194 persons) aged 30-39 in order to estimate possible functions of ascorbic acid in the prevention of the disease. Serum ascorbic acid had an inverse and the strongest association with systolic blood pressure among the risk factors including blood pressure, total cholesterol, triglyceride, gamma-GTP and obesity. The association was independent of the other variables tested. When the subjects were divided into three different serum ascorbic acid level groups, the prevalence of hypertension (140/90 mmHg and above) was decreased with an increase in the ascorbic acid level. The close relationship of serum ascorbic acid and blood pressure observed in the study suggests that ascorbic acid may have a preventive function against hypertension, or a low ascorbic acid status in hypertensives may promote the further development of arteriosclerosis by the lack of favorable effect of ascorbic acid on lipid metabolism and others.
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PMID:Inverse association of serum ascorbic acid level and blood pressure or rate of hypertension in male adults aged 30-39 years. 615 42


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