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

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

Studies were performed to evaluate the metabolic changes of brown adipose tissue (BAT) in rats with hypothalamic obesity (VMNL). In vitro 14C-palmitate oxidation and incorporation into triglycerides were similar in VMNL and control rats. However, protein and fatty acid content and incorporation of 14C-palmitate into phospholipid were significantly less in both hyperphagic and normophagic VMNL rats. In order to assess in vivo BAT lipogenesis, rats were injected with 3H2O. Plasma H2O incorporation into BAT lipids was significantly greater in VMNL rats. Likewise, BAT lipid content was higher in obese rats. In another experiment BAT was incubated with U-14C-glucose to evaluate glucose utilization by BAT. 14C-glucose was oxidized and incorporated into both lipids and glycogen more rapidly by obese than by normal rat BAT. Glycogen content was greater in VMNL rats. Tissues were also incubated with 1-14C-pyruvate and 2-14C pyruvate. Pyruvate incorporation into glyceride glycerol and oxidation of 2-14C pyruvate through the Krebs cycle were similar in both obese and control rats. However, the incorporation of pyruvate into glyceride fatty acids was increased in VMNL rats. The results indicate that both fatty acid and lipid synthesis are increased in BAT of obese rats whereas lactate production is decreased and Krebs cycle activity is normal. Some of these changes appear to be independent of the level of food intake.
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PMID:Brown adipose tissue metabolism in hypothalamic-obese rats. 682 81

Rats were made to overeat and gain weight (about 50 g) by long-acting protamine zinc insulin (PZI) treatment. When the PZI treatment was stopped, the rats ate much less than normal for at least seven days. During recovery from PZI-induced obesity, negative correlations were observed between food intake and plasma levels of the fat metabolites, free fatty acids, glycerol, and ketone bodies. A similar but smaller effect was observed during recovery from dietary obesity (about 15 g). The plasma fat metabolites may be the blood-borne signals which suppress hunger under these conditions.
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PMID:Reversible obesity and plasma fat metabolites. 683 44

In order to test the hypothesis that the fat metabolites are the blood-borne signals which suppress hunger during recovery from reversible obesity, experiments were designed to manipulate plasma fat metabolite levels directly. In order to elevate plasma glycerol levels, glycerol was infused intravenously into relatively unrestrained rats for 36 hours; this treatment greatly increased plasma glycerol levels but reduced voluntary food intake only slightly. Similar results were obtained when glycerol was mixed with powdered rat food. These results suggest that glycerol is not the "lipostatic hormone" although it may contribute to regulation. Similar experiments with a synthetic precursor of the ketone bodies (1,3 butanediol), suggest that the ketone bodies contribute to the decrease in food intake after reversible obesity, but cannot be a complete explanation. Dietary fat consumption raised plasma free fatty acid (FFA) levels to the range seen during recovery from reversible obesity, suggesting that plasma FFAs may be a blood-borne signal of fat utilization in both cases. Intralipid, a synthetic triglyceride emulsion designed for intravenous administration, also increased plasma FFA levels but suppressed food intake by less than predicted. However, Intralipid may tend to cause spuriously high plasma FFA readings for reasons which are discussed. These results suggest that plasma fat metabolites, especially FFAs, may be blood-borne signals which contribute to the voluntary dieting after reversible obesity.
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PMID:Plasma fat metabolites and hunger. 683 45

Hormone and metabolite profiles were investigated over a 12-hr period in six patients with Cushing's syndrome, ten age- and sex-matched normal controls, and six moderately obese subjects matched for weight with the patient group. Mean diurnal plasma cortisol levels were 563 +/- 74 nmole/liter in the patients, 275 +/- 22 nmole/liter in normal controls and 241 +/- 32 nmole/liter in obese subjects, with total loss of diurnal changes in Cushing's syndrome. Fasting blood glucose concentration was similar in all groups although mild hyperglycemia occurred after meals in the Cushing's patients compared with normal and obese subjects (mean 12-hr blood glucose: Cushing's 6.31 +/- 0.39 mmole/liter; normal controls, 5.32 +/- 0.14 mmole/liter, p < 0.01; obese subjects, 5.41 +/- 0.18 mmole/liter, p < 0.05) despite marked hyperinsulinemia (mean 12-hr serum insulin: Cushing's 57.3 +/- 18.2 mU/liter; normal controls, 19.7 +/- 2.5 mU/liter, p < 0.02; obese subjects, 18.1 +/- 4.0 mU/liter, p < 0.05). Concentrations of the gluconeogenic precursors lactate, pyruvate, and alanine were raised in Cushing's syndrome, particularly postprandially. Plasma nonesterified fatty acids (NEFA), blood glycerol, and blood ketone body concentrations were comparable in all three groups although the normal diurnal variation in circulating NEFA and ketone body levels was lost in Cushing's syndrome. Serum triglyceride (TG) concentrations were grossly elevated in the Cushing's patients (mean 12-hr serum TG: Cushing's 3.51 +/- 1.23 mmole/liter; normal controls 0.89 +/- 0.19 mmole/liter, p < 0.02; obese subjects, 0.93 +/- 0.23 mmole/liter, p < 0.05) and correlated positively with serum insulin levels. Plasma glucagon concentrations were raised in Cushing's syndrome (mean 12-hr plasma glucagon: Cushing's 23.2 +/- 3.7 pmole/liter; normal controls 12.3 +/- 1.5 pmole/liter p < 0.01; obese subjects 12.2 +/0 2.0 pmole/liter, p < 0.02) and correlated positively with the serum cortisol but not with blood alanine, suggesting that some stimulatory factor other than alanine was responsible. The metabolic effects of chronic glucocorticoid excess thus may not be explained on the basis of obesity alone. Compensatory hyperinsulinemia limits the disturbance of carbohydrate and lipid metabolism in Cushing's syndrome but may be important in production of the hypertriglyceridemia observed.
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PMID:Hormonal and metabolic rhythms in Cushing's syndrome. 700 Nov 75

Pima Indians have a high prevalence of hyperinsulinemia, obesity, and diabetes, but they have low plasma cholesterol levels, reduced low density lipoprotein synthesis, and little arteriosclerotic heart disease. To investigate lipoprotein metabolism further in this group, very low density lipoprotein (VLDL) metabolism was studied, using [3H]glycerol as an endogenous precursor of triglyceride (TG) synthesis, in 15 obese Pima nondiabetic males and compared to that of 10 obese and 13 normal weight, normolipidemic, nondiabetic Caucasian males. The resultant kinetic data were analyzed using a multicompartmental model which includes two pathways for VLDL-TG synthesis and a process of stepwise delipidation for VLDL catabolism. As compared to obese Caucasians, the obese Pimas had a lower rate of VLDL-TG synthesis, and a lower proportion of slow pathway for synthesis. The fractional catabolic rate in the Pimas was higher than in either Caucasian group, a larger proportion of VLDL-TG was delipidized at each step, and particle residence time was shorter. When the relation between VLDL-TG metabolism and plasma insulin was examined, plasma insulin levels in the Pima were not correlated with VLDL-TG synthetic rates, catabolic rates, or plasma pools. On the other hand VLDL-TG synthetic rates were correlated with plasma free fatty acid levels. Thus, in this population with low plasma lipids and reduced arteriosclerotic heart disease, VLDL-TG synthesis is low, VLDL-TG catabolism is accelerated, and VLDL pools appear to be insensitive to the influence of body weight and hyperinsulinemia.
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PMID:Studied of very low density lipoprotein triglyceride metabolism in an obese population with low plasma lipids: lack of influence of body weight or plasma insulin. 700 43

Weanling male Sprague-Dawley rats received bilateral electrolytic lesions in the ventromedial hypothalamic nuclei (VMNL rats); sham-operated rats served as controls. For 28 post-operative d all animals were fed three equicaloric [16.9 kJ/g (4.03 kcal)] diets with different amounts of macronutrients in each (HCD = high-carbohydrate diet, HFD = high-fat diet and HPD = high-protein diet). VMNL rats selected more than controls from HCD (P less than 0.05) and HFD (P less than 0.01) but similar amounts from the HPD. The total intake from all three diets was greater (P less than 0.001) than that of the controls, but in percent of total diet intakes, VMNL selected proportions comparable to the controls. In terms of macronutient intake, VMNL rats ingested more than controls from each (carbohydrate, P less than 0.001; fat, P less than 0.05; protein, P less than 0.01). Again, in percent of total macronutrient intake, they ingested proportions comparable to the controls. Lee Index (P less than 0.001) was greater and body weight gain/kJ (kcal) smaller (P less than 0.001) in VMNL rats than in controls. However, body weight gains were normal. For the following 14 d, one group of VMNL rats and one control group continued to self-select from the three diets while another VMNL and control group received lab chow [14.2 kJ/g (3.39 kcal)]. Analysis of variance showed a lesion effect for the Lee Index (P less than 0.001) and Lee Index gain /kJ(kcal) (P less than 0.01) but body weight gains and caloric intake were normal among the groups, ie the VMNL rats switched to chow decreased their caloric intake to control levels. On sacrifice, white and brown fat percent protein (P less than 0.001 for both), carcass lipid (P less than 0.001) and protein (P less than 0.01) and plasma insulin (P less than 0.001) showed lesion effects, but there were no differences among the groups in plasma glucose, glycerol, total protein and free-fatty acids. Availability of palatable diets immediately following VMN lesion placement in weanling rats will result in hyperphagia that after one month recedes to normophagia, whether the rats are fed palatable or less palatable diets. Availability of a less palatable diet (chow) following presentation of palatable diets will not result in diminished caloric intake, body weight, obesity and hyperinsulinemia.
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PMID:Hypothalamic obesity in the weanling rat: dietary self-selection, actual macro-nutrient intake, caloric regulation and response to subsequent low palatability diet. 712 49

Fat cell hypertrophy occurs in most forms of obesity. In the obese Zucker rat, fat cell hypertrophy and increased lipoprotein lipase activity (LPL) are the earliest known signs of obesity. We studied the regulation of fat cell size in the obese Zucker rat by measuring changes in fat cell LPL activity and lipolysis in response to an overnight fast in 6- and 14-wk-old lean and obese rats. At both ages, fed obese rats had significantly increased fat cell size, LPL activity, and basal glycerol release in three adipose tissue depots compared to fed lean rats. Obese rats decreased LPL activity in response to fasting, but levels always remained equal to or greater than those in fed lean rats. Obese rats also showed a reduced lipolytic response to fasting. Thus, the obese rat after an overnight fast could not produce a coordinated response to fasting similar to the lean rat, and its homeostatic adjustments to this mild stimulus favored preservation of its enlarged fat cell size.
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PMID:Adipose tissue lipoprotein lipase and glycerol release in fasted Zucker (fa/fa) rats. 724 71

In rats allowed access to food, and in food-deprived rats, fenfluramine (20 and 100 mg kg-1) and amphetamine (10 and 20 mg kg-1) provoked a hypotriglyceridaemic effect. No changes in plasma cholesterol concentration were observed. The time course of the absorption of a lipid load differed according to the nutritional status of the animals; being bellshaped under fed, and curvilinear under fasted, conditions. However, absorption under both nutritional conditions was inhibited by amphetmine and fenfluramine. When rats which had received the test compounds were administered glycerol trioleate containing a tracer dose of glycerol [1-14C]-trioleate or [2-3H]-glycerol trioleate, there was an inhibition in the increase of plasma radioactivity only in the case when the fatty acid contained the radioactive label. The net effect of lipid absorption was a transfer of dietary lipid from the gut to adipose tissue stores. There was never more than 5 per cent of the administered load in the liver. These observations indicate that amphetamine and fenfluramine may have acute effects in reducing circulating triglycerides, separate from the effects on lipid absorption from the gut. In this latter, the palmitoyl-CoA monooleinacyltransferase enzyme probalby plays a key role and appears a major target of the overall anti-obesity of fenfluramine.
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PMID:Anti-hypertriglyceridaemic activity of some phenylethylamine anorectic compounds. 739 2

Lactate and glycerol turnover is enhanced in obesity and NIDDM. To evaluate the influence of NIDDM on subcutaneous adipose tissue metabolism microdialysis combined with 133Xe clearance and measurements in arterialized plasma were carried out using samples of subcutaneous abdominal fat from nine obese NIDDM subjects (glucose, 7.9 +/- 0.7 mmol L-1) (mean +/- SEM) and nine obese non-diabetic subjects (glucose, 4.9 +/- 0.1) matched for age, BMI and body fat. After an overnight fast arterialized plasma levels were 1145 +/- 110 vs. 876 +/- 59 mumol L-1 (P < 0.05) for lactate and 75 +/- 10 vs. 66 +/- 8 mumol L-1 for glycerol in the diabetic and control group, respectively. The corresponding abdominal subcutaneous interstitial lactate and glycerol concentrations were 1278 +/- 63 vs 1107 +/- 64 mumol L-1 and 314 +/- 28 vs. 311 +/- 17 mumol L-1, respectively. However, adipose tissue blood flow in the same region was lower in NIDDM subjects (1.5 +/- 0.2 vs 2.4 +/- 0.3 mL 100 g-1 min-1) (P < 0.05). Consequently, apparent subcutaneous lactate and glycerol release, estimated according to Fick, were not statistically different in the two groups (1.8 +/- 0.4 vs 2.4 +/- 0.8 and 2.1 +/- 0.4 vs 3.1 +/- 0.5 mumol kg-1 min-1 in NIDDM and control subjects, respectively). Thus, in the post-absorptive state apparent lactate and glycerol release by the abdominal subcutaneous tissue in obese NIDDM subjects was similar to that in a matched group of obese non-diabetic controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Microdialysis assessment of adipose tissue metabolism in post-absorptive obese NIDDM subjects. 758 14


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