Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Lack of sex differences in high density lipoproteins in Pima Indians. Studies of obesity, lipase activities, and steroid hormones. 359 76

A physiological in vivo increase of plasma free fatty acid concentration after an overnight fast was found to be accompanied by a rise of the non-protein bound estradiol fraction. A similar increase was observed after lipase activation by the i.v. injection of 500 IU heparin in 5 healthy non-fasting subjects. In vitro studies showed a direct relationship between non-protein bound estradiol and the concentration of linoleate, linolenate, and arachidonate both in undiluted serum and in Ringer's solution containing human serum albumin (45 g/liter). Moreover, the estradiol sex hormone binding globulin complex bound to a solid concanavalin A-Sepharose matrix was markedly dissociated by oleate and even more by linoleate, linolenate, or arachidonate. These results suggest that physiological diurnal elevations in plasma free fatty acids which are amplified by high fat consumption, obesity, and stress may imply major proportional increases of available estradiol, exerting a promotional effect on breast and endometrial cancer over the years.
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PMID:Free fatty acid concentrations correlated with the available fraction of estradiol in human plasma. 369

Lipoprotein lipase is a key enzyme of lipid metabolism that acts to hydrolyze triglycerides, providing free fatty acids for cells and affecting the maturation of circulating lipoproteins. It has been proposed that the enzyme plays a role in the development of obesity and atherosclerosis. The human enzyme has been difficult to purify and its protein sequence was heretofore undetermined. A complementary DNA for human lipoprotein lipase that codes for a mature protein of 448 amino acids has now been cloned and sequenced. Analysis of the sequence indicates that human lipoprotein lipase, hepatic lipase, and pancreatic lipase are members of a gene family. Two distinct species of lipoprotein lipase messenger RNA that arise from alternative sites of 3'-terminal polyadenylation were detected in several different tissues.
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PMID:Human lipoprotein lipase complementary DNA sequence. 382 7

In vitro experiments using both primary fetal hepatocyle cultures and adipoblast cultures have demonstrated that the presence of the fa gene is associated with decreased synthetic capacity, when compared to wild-type cultures. These results are in contrast to the elevated lipogensis and lipoprotein-lipase activities found in vivo in young adult obses (fafa) Zucker rats compared to their lean littermates. These studies used adipoblast cultures to address three possible explanations for these in vitro-in vivo differences: 1) FaFa and fafa adipoblast cultures represent different cell populations with intrinsically different abilities to differentiate, ie, to lipid-fill. 2) The decreased synthetic capacities in fafa vs FaFa adipoblast cultures are specific to cultures derived from the epididymal pad. 3) Cultured adipoblasts produce factor(s) that affect adipoblast differentiation in vitro. Results indicate that 1) the rate of differentiation is slower in fafa than in FaFa adipoblasts 2) there are depot-related differences in lipid metabolism, but these differences do not negate the in vitro association between the fa gene and decreased synthetic capacity and 3) FaFa epididymal-derived adipoblasts produce a factor(s) that affects inguinal-derived adipoblast differentiation and/or growth in vitro. Thus it is important to take both the site of cell origin and culture conditions into consideration when using in vitro systems as an approach to understanding complex in vivo disorders, such as obesity in the Zucker fafa rat.
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PMID:Adipoblasts from the Zucker fafa rat. 384 Jul 74

The presence of a lipidbound inhibitor in adipose tissue of rats with hypothalamic obesity may explain the failure of the tissue to release fatty acids on epinephrine stinmulation. Aqueous extracts of tissue from obese animals showed no deficiency of lipase activity, but when whole homogenates of epididymal fat from lean and obese animals were mixed, 25 percent tissue from obese animals reduced by 73 percent the release expected from tissue of lean controls.
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PMID:Lipolysis in homogenates of adipose tissue: an inhibitor found in fat from obese rats. 600 38

Weanling male rats with ventromedial hypothalamic lesions (VMNL rats) and sham-operated controls were killed 1, 2, 4, and 5 weeks postoperatively. The VMNL rats developed normophagic hypothalamic obesity in the presence of normal body weight and reduced linear growth. In both VMNL and control rats, pancreatic weight and protein content increased with time but were lower in the lesioned animals. Pancreatic DNA content was arrested in VMNL rats and remained so during the remainder of the experiment. The only significant enzyme changes (trypsinogen, amylase, and lipase) were evident in higher trypsinogen concentration in VMNL rats during 2 and 4 weeks after lesion production. In view of previous data on both hypophysectomized and VMNL rats and the known role of the ventromedial hypothalamic nucleus in neuroendocrine and neuroautonomic function, it is speculated that the changes observed here are in part due to disruption of neuroendocrine and in part due to disturbance of neuroautonomic control systems.
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PMID:Pancreatic growth and enzyme profiles in weanling rats with normophagic hypothalamic obesity. 608 27

The effects of treatment on plasma total triglyceride, total cholesterol, and plasma postheparin lipase activities have not been evaluated in non-insulin-dependent diabetic (NIDD) subjects without a coexisting familial lipid disorder. In 49 untreated NIDD subjects, there was a linear relationship between glycosylated hemoglobin (GHb) and triglyceride (r = 0.35, P less than 0.02). This correlation was improved after adjusting for the effects of obesity by a partial correlation analysis. After therapy, there was a significant relationship between the change in GHb and the change in triglyceride. To determine whether changes in lipid removal from plasma may contribute to the decrease in plasma lipid concentrations during treatment, the plasma postheparin lipoprotein lipase and hepatic lipase activities were evaluated in a subgroup (N = 8) of these NIDD subjects before and after 1 and 3 mo of therapy. Plasma postheparin hepatic lipase activity in the NIDD subjects was not different from that observed in six normal control subjects and did not change during therapy. In contrast, plasma postheparin lipoprotein lipase activity was lower in the untreated NIDD subjects than in the control subjects. Analysis of the two phases (early and late) of the postheparin lipoprotein lipase activity in plasma showed that the abnormal early phase in untreated NIDD corrected to normal values in less than a month, but the late phase was not corrected until the 3-mo measurement. These findings suggest that some NIDD subjects have a defect in heparin releasable lipoprotein lipase activity, which is reversed with improved glycemic control.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The response of plasma triglyceride, cholesterol, and lipoprotein lipase to treatment in non-insulin-dependent diabetic subjects without familial hypertriglyceridemia. 635 82

A total of 128 patients with alimentary obesity were examined in the course of the treatment. There was a significant elevation in blood serum of total and free cholesterol, its esters, free fatty acids, beta-lipoproteins, and a decrease in the activity of serum lipase. The correlation of cholesterol esters to phospholipids was found to be disordered. Eighty patients demonstrated, after treatment with chloride sodium bromoiodine baths combined with hypocaloric diet and exercise therapy, a favourable clinical time course and normalization of the majority of lipid metabolism indicators, with an increase in serum lipase activity. Twenty-five patients, who received fresh baths under similar conditions, demonstrated less pronounced shifts in lipid metabolism, which were not always significant. The treatment complex including phepranon also gave rise to the normalization of the majority of lipid metabolism indicators. However, one-third of cases developed serious side effects.
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PMID:[Dynamics of lipid metabolism in the combined treatment of alimentary obesity]. 651 36

The relationship between obesity and alterations in adipose tissue metabolism and lipid transport was studied in fourteen obese subjects before and after a weight reduction of 4-22 kg. Blood glucose and plasma insulin patterns after peroral glucose intake improved significantly, and plasma glucagon levels decreased markedly after treatment. Plasma triglyceride and total cholesterol levels were not altered, but there was a 20% (P less than 0.05) increase in HDL concentrations. Plasma free fatty acid and glycerol concentrations decreased, in parallel to a decrease in lipolysis rate in vitro. Lipoprotein lipase and hepatic lipase activities in postheparin plasma, as well as the intravenous fat tolerance test, were normal and did not change significantly after weight loss. Lipoprotein lipase activity in adipose tissue, expressed per cell, was elevated and did not change after weight reduction. Also, the enzyme activity did not increase after glucose intake before or after treatment. The lack of effect on lipoprotein lipase activity and regulation in combination with significant improvements of other aspects of lipid and glucose transport is consistent with the view that alterations in LPL activity and regulation may represent an early and possibly primary defect in the development of obesity.
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PMID:Effects of weight reduction on plasma lipoproteins and adipose tissue metabolism in obese subjects. 680 Aug 25

Adipose tissue and muscle lipoprotein lipase and postheparin hepatic and lipoprotein lipase activities have been measured in a group of 21 Pima Indian males over a wide range of body weight to determine the relationship between obesity and these lipase activities. There was a significant positive correlation between adipose tissue lipoprotein lipase and obesity; muscle and postheparin lipoprotein lipase and hepatic lipase were not related to degree of obesity. Fasting insulin levels were not related to any of the measurements of lipase activity. There were racial differences in adipose and postheparin lipoprotein lipase activities; both were significantly lower in the Pimas as compared with a group of weight-matched Caucasian males. Lipase activities were remeasured in eight subjects after a period of weight reduction including several weeks of stabilization at the reduced weights. After the period of weight reduction adipose tissue lipoprotein lipase declined in all subjects. Hepatic lipase also declined in all but two patients. Muscle and postheparin lipolytic activities were not affected by weight loss. The data indicate that (a) there are racial differences in adipose tissue lipoprotein lipase; and (b) the elevated adipose lipoprotein lipase associated with obesity, like many other biochemical variables in the obese state, returns toward normal after weight reduction.
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PMID:Characterization of lipase activities in obese Pima indians. Decreases with weight reduction. 711 15


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