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

Chronic treatment of rats with dexfenfluramine decreased the concentrations of circulating corticosterone, fatty acid, glycerol, and triacylglycerol after feeding a test load of fructose. It also decreased the rise in adrenalin in the blood of rats that were anaesthetized with urethane. These effects of dexfenfluramine probably result from changes in the metabolism of 5-HT in the CNS and consequent alterations in hormonal balance. It is proposed that the long-term metabolic effects of dexfenfluramine could be explained by a decrease in the effectiveness of stress hormones (e.g., glucocorticoids, corticotropin, catecholamines, glucagon) in regulating metabolism since these hormones antagonize many of the actions of insulin. This hypothesis also identifies the possibility that the ability of dexfenfluramine to decrease an exaggerate stress response could alleviate some of the potential risk factors associated with atherosclerosis including obesity and maturity onset diabetes.
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PMID:Metabolic and hormonal effects of dexfenfluramine on stress situations. 318 Jan 10

(1) Rats were fed on diets enriched with sucrose, beef tallow or corn oil and treated for 11-16 days with 50 mg of benfluorex per kg of body weight. By these times the growth rate and food intake were not significantly different from those of control rats. (2) Benfluorex approximately halved the concentration of circulating triacylglycerol in rats fed the beef tallow or sucrose diets. (3) It did not significantly alter the total lipoprotein lipase activity in diaphragm, heart and adipose tissue. (4) The clearance of triacylglycerols from chylomicrons exhibited two t 1/2 values of about 0.6 and 6.9 min in rats fed the beef tallow diet. Benfluorex did not significantly alter these values. (5) Benfluorex did not significantly alter the rate of appearance of triacylglycerol in the blood of rats injected with Triton WR 1339 to block triacylglycerol uptake. It did, however, decrease the rise in circulating glucose which presumably resulted from the stress of the procedure. (6) Benfluorex decreased the extent and duration of the rise in serum corticosterone when rats maintained on the corn oil diet were fed acutely with fructose. It also decreased the circulating concentrations of glycerol, triacylglycerol and glucose after fructose feeding. (7) Rats fed on the corn oil diet and then treated with benfluorex had lower concentrations of circulating glucose, triacylglycerol, glycerol and fatty acids after being injected with 2-deoxyglucose. (8) It is proposed that some of the long-term hypoglycaemic and hypotriglyceridaemic effects of benfluorex could be mediated indirectly through changes in endocrine balance, perhaps via the serotonergic system and in particular, by decreasing the effects of stress hormones relative to insulin. The implications of these findings are discussed in relation to controlling metabolism in stress conditions and for the management of obesity, diabetes and atherosclerosis.
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PMID:Effects of chronic administration of benfluorex to rats on the metabolism of corticosterone, glucose, triacylglycerols, glycerol and fatty acid. 334 1

The thermic response to noradrenaline infusion was measured by indirect calorimetry in 40 newly referred obese subjects and 19 lean controls. A marked variation in response was found, more so in the obese than in the lean. In the lean group the lowest noradrenergic thermic response was 12.8 kJ but in the obese group 26 per cent had a thermic response less than this. When the thermic response to noradrenaline is expressed as a percentage of the resting metabolic rate the response was significantly (P less than 0.002) lower in the obese, 8.5 (s.d. 6.0) per cent compared with 13.8 (s.d. 5.1) per cent in the lean. The lowest value in the lean group was 7.8 and 42 per cent of the obese group had lower values. The thermic responses in the obese group did not correlate with glucose:insulin ratios measured both fasting and in response to oral glucose, or with the cumulative rises of either free fatty acids or glycerol during the noradrenaline infusion. Hence the majority of obese subjects have a 'normal' response to infused noradrenaline, but there is a subgroup who do have a blunted response. This may explain to some extent the conflicting reports in the literature regarding the presence of otherwise of a thermic defect in obesity.
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PMID:Heterogeneity of noradrenergic thermic responses in obese and lean humans. 339 41

Overfeeding increases the thermogenic response of norepinephrine (NE) in normal but not in certain genetically obese rodents. It has been suggested that human obesity may be associated with a similar thermogenic defect. To determine whether there are differences in the thermogenic sensitivity to NE in human obesity, energy expenditure in response to graded infusions of NE (0.05, 0.10, 0.15, 0.20 micrograms/min/kg fat-free mass) was measured in six lean and six obese subjects (9.5 +/- 1.8 v 36.3 +/- 3.8% body fat P less than 0.005). Resting metabolic rate (RMR), thermogenic response to NE, and thermogenic response to exercise were measured during weight maintenance and during the third week of feeding 1000 extra Kcal/d in the lean and obese subjects. These components of energy expenditure were also measured in the obese subjects during the third week of a 589 Kcal/d diet. Resting metabolic rate increased during overfeeding in lean (6.6%, P less than 0.05) but not in the obese subjects (2.7%, P = NS) and fell during underfeeding in the obese (-9.1%, P less than 0.02). There was a logarithmic increment above baseline in VO2 v plasma NE concentration during the NE infusions (r = 0.75, P less than 0.005) in lean subjects which was unaltered by overfeeding. The obese exhibited equivalent VO2 responses to NE to that measured in the lean. Supine plasma NE concentrations were lower but metabolic clearance rates (MCR) of NE were similar in the obese compared to lean subjects during both weight maintenance and overfeeding. Overfeeding minimally increased plasma concentration but not MCR of NE in both groups. The thermogenic response to exercise was similar in the lean and obese subjects and was unaltered by overfeeding or underfeeding. The increments in plasma glycerol and free fatty acid in response to the NE infusions were proportional to the total fat mass of each individual and were greater in the obese subjects. Overfeeding partially suppressed the lipolytic response to NE in both groups and underfeeding increased the lipolytic response in the obese. There are no differences in thermogenic responses to NE in human obesity to account for excessive fat deposition. Overfeeding does not increase the thermogenetic responses to NE in humans as has been reported in small mammals.
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PMID:Metabolic studies in human obesity during overnutrition and undernutrition: thermogenic and hormonal responses to norepinephrine. 345 75

The present work was undertaken to study the effect of nutritional obesity induced by a high fat diet on the consumption of glycogen and glycerides in rat liver and diaphragm. Groups of rats were fed for five weeks from weaning either a fat-rich-carbohydrate (CHO)-poor diet, or a CHO-rich-fat-poor diet. Basal plasma glucose and free fatty acids (FFA) were significantly increased in the animals adapted to the fat-rich diet. Half of the rats were submitted to a 48-h fast. After fast, basal plasma glucose and immunoreactive insulin (IRI) fell significantly, whereas plasma FFA levels were higher than in the group fed the CHO-rich-fat-poor diet. In the liver, glycogen concentration fell in both groups after fast, with a glycogen breakdown of 1930 +/- 244 mumole glycogen glucose/liver in the fat-fed group vs 4636 +/- 216 mumole/liver in the CHO-fed group. Glycerides fell by 750 +/- 68 mumole glyceride glycerol/liver in the fat-fed rats while remaining unchanged (increased by 82 +/- 57 mumole/liver) in the CHO-fed group. In the diaphragm glycogen concentration also fell in both groups, with a glycogen breakdown of 6.0 +/- 0.3 mumole glycogen glucose/g wet tissue in the fat-fed rats vs 15.2 +/- 1.4 mumole/g wet tissue in the CHO-fed animals. Glycerides fell by 23.1 +/- 4.0 mumole/g wet diaphragm in the CHO-fed animals. The lower breakdown of glycogen in both liver and diaphragm of fat-fed rats demonstrates a decreased utilization of glycogen during fast, with energy consumption originating in larger part from triglycerides.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Study on the effect of a high fat diet on diaphragm and liver glycogen and glycerides in the rat. 351 28

Weanling male Sprague-Dawley rats received bilateral electrolytic lesions in the dorsomedial hypothalamic nuclei (DMNL rats); sham-operated rats served as controls. All animals were fed lab chow for 15 postoperative days. At that time they were subdivided into two groups each. One DMNL and one control group continued to be fed lab chow until the termination of the experiment on postoperative day 116. A second DMNL and control group were fed a high-fat diet and 32% sucrose solution (HF/SS diet). All DMNL rats showed reduced body weight and linear growth, but the HF/SS diet depressed these parameters further below the levels of the chow-fed groups. Both DMNL and control rats fed HF/SS had more carcass fat, heavier epididymal fat pads, more carcass fat per calories eaten, higher plasma levels of glucose, glycerol and free fatty acids but lower insulin levels than chow-fed DMNL rats and controls. This occurred in the face of lower body weights and caloric intake. Neither growth hormone nor insulin showed lesion effects. Rats with DMNL exhibited the same inverse relationship between plasma insulin and free fatty acids as controls. The data indicate that DMNL rats respond to the HF/SS diet essentially like sham-operated controls, i.e., they develop dietary obesity. Although they do show some small deficits, their lipogenic capacity is actually significantly greater than that of HF/SS-diet fed controls.
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PMID:Effect of palatable diet on growth, caloric intake and endocrine-metabolic profile in weanling rats with dorsomedial hypothalamic lesions. 354 85

Two experiments examined the hypophagia that occurs when rats are switched from a high-fat to a low-fat diet. In the first experiment, rats fed a high-fat diet for eight weeks weighed 79 g more than rats fed a low-fat diet. Removal of the high-fat diet led to reduced food intake for at least four weeks. Reducing the body weight of the rats by a 24 hour fast did not alter the time course of the hypophagia. Plasma levels of free glycerol, free fatty acids and ketones were elevated during and after feeding the high-fat diet; suggesting that feeding a high-fat diet increases fat oxidation even after the high-fat diet is withdrawn. In the second experiment, feeding rats the high-fat diet for four weeks increased body weight and body fat. Starving the rats for two days after feeding the high-fat diet did not alter subsequent hypophagia and did not alter the percentage of body fat. This pattern of results is similar to that previously seen following termination of obesity-inducing insulin treatment. The results are consistent with the idea that a persistent increase in fat oxidation is responsible for the hypophagia.
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PMID:Hypophagia following dietary obesity. 378 6

There is some evidence that blockade of alpha 2-adrenoceptors on adipocytes may lead to an increase in lipolysis, We have therefore carried out a double blind comparative study of the effects of the selective alpha 2-antagonist yohimbine in human obesity. Nineteen obese volunteers participated in the study. Subjects were randomly allocated to the yohimbine group (n = 10, 18 mg yohimbine/day), or to the placebo group (n = 9). All subject were maintained on a hypocaloric diet (1000 kcal/day) during the 8 weeks of the study. There was no difference between the two groups with respect to either body weight, blood pressure supine and erect or heart rate during the different phases of the study. We found no difference in the lipid parameters (triglycerides, cholesterol, glycerol, beta-OH-butyrate, acetoacetate and free fatty acids) between the two groups. These results suggest that at the dose used the yohimbine does not influence the function of the alpha 2-adrenoceptors on the adipocytes; does not increase the lipolysis and does not represent an effective treatment of obesity.
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PMID:[Lack of efficacy of yohimbine in the treatment of obesity]. 379 78

In this report, kinetic studies of plasma very low-density lipoprotein-triglyceride (VLDL-TG) were examined in five brothers (three affected and two unaffected) from a family with primary hypertriglyceridemia. Synthesis and catabolism of VLDL-TG were studied by in vivo labelling of plasma TG with 3H-glycerol, and multicompartmental analysis of the plasma die-away curves. Results of the kinetic studies revealed the following information: (1) one brother, who had the highest plasma TG level and was obese, had both overproduction and a reduced fractional catabolic rate (FCR) of VLDL-TG; (2) second brother, who had moderate hypertriglyceridemia, had a low FCR and high-normal synthesis of VLDL-TG; (3) a third, who had only mildly elevated TG, had a low FCR and normal synthesis of VLDL-TG; and (4) the two normolipidemic brothers had neither overproduction nor decreased FCR of VLDL-TG. The composition of the soluble apoproteins of VLDL was normal. The apoprotein E phenotypes were E4/3 in four brothers, and E3/2 in the fifth. We have reached the following conclusions regarding this family: (1) the common kinetic abnormality of VLDL-TG metabolism in the hypertriglyceridemic brothers was a low clearance of VLDL-TG; (2) impaired catabolism of VLDL could not be explained by the apoprotein C or E patterns; and (3) the most severe hypertriglyceridemia occurred when the decreased FCR was present in conjunction with VLDL-TG overproduction due to obesity. Thus, a moderate defect in catabolism of plasma TG appears to be responsible for one familial form of primary hypertriglyceridemia.
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PMID:Impaired catabolism of very low-density lipoprotein-triglyceride in a family with primary hypertriglyceridemia. 388 62

The health consequences of obesity in adults encompass both metabolic and cardiovascular complications. Pregnancy in obese women also has a particular set of problems. For the obese pregnant woman, these include weight gain less than 5.4 kg, chronic hypertension and superimposed preeclampsia, gestational diabetes, multiple gestation, and the potential for a macrosomic child. The combination of obesity and maternal diabetes does not appear to have an additive effect on the excessive growth of infants of obese mothers. Furthermore, despite inadequate weight gain, hypertension, and multiple gestation, infants of obese mothers are usually born with a greater birth weight than those of nonobese women. In addition, the incidence of intrauterine growth retardation is lower after an obese pregnancy. Neonates born to obese mothers have increased risk for birth asphyxia and birth trauma. Recently infants born to obese women were noted to have transient neonatal fasting asymptomatic hypoglycemia. Hyperinsulinism is not present in the infants of obese mothers; thus, alternate fuel mobilization (free fatty acids, glycerol, ketones) may respond to the hypoglycemic stimulus. Suggestions and rationale for the management of the pregnant obese woman, fetus, and newly born infant are discussed in the text.
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PMID:Perinatal problems of the obese mother and her infant. 389 77


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