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

The antilipolytic effect of insulin was studied in 9 obese and 10 age- and sex-matched subjects of normal weight. Isolated fat cells were taken before and 1 h after an 100 g oral glucose load. Insulin inhibition of basal and isoprenaline-induced rates of lipolysis were determined by using a sensitive bioluminescent glycerol assay. When compared with the controls, the obese group showed a lower glucose tolerance, a higher insulin secretion, and a lower specific insulin receptor binding per adipocyte surface area, which would suggest an insulin-resistant state. Before oral glucose, however, the sensitivity of the antilipolytic effect of insulin was enhanced 10-fold in obesity (P less than 0.01), but the maximum antilipolytic effect was not altered. Glucose ingestion induced a 10-25-fold increase in insulin sensitivity (P less than 0.01) and a 10% but not significant increase in specific adipocyte insulin receptor binding in the nonobese group. In the obese group, however, neither the insulin binding nor the antilipolytic effect of the hormone was increased by oral glucose. After oral glucose, insulin sensitivity was similar in the two groups. The concentration of the hormone which produced a half maximum effect was about 1 microU/ml. Similar results were obtained with insulin inhibition of basal and isoprenaline-stimulated glycerol release. It is concluded that, after an overnight fast, the sensitivity of the antilipolytic effect of insulin is markedly enhanced in adipocytes of "insulin-glucose resistant" obese subjects, presumably because of alterations at postreceptor levels of insulin action. In obesity, the antilipolytic effect of insulin seems normal after glucose ingestion. Furthermore, in adipocytes of subjects of normal weight, oral glucose rapidly stimulates the sensitivity of the antilipolytic effect of insulin, apparently because of changes at postreceptor sites. This short-term regulation of insulin action following the ingestion of glucose does not seem to be present in obesity.
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PMID:Influence of obesity on the antilipolytic effect of insulin in isolated human fat cells obtained before and after glucose ingestion. 636 86

The effect of neonatal sympathectomy with guanethidine (50 mg/kg for 3 wk) on the development of diet-induced obesity (DIO) was assessed by raising guanethidine-(G) or saline-treated (S) Sprague-Dawley rats in small litters (4-5 pups/dam) and feeding a high-calorie diet from weaning (n = 29-30) or by raising similarly treated rats in normal litters (10 pups/dam) and feeding chow from weaning (n = 29-30). Sympathectomy depleted norepinephrine (NE) levels 65-98% in all organs except the adrenals and brain but had no statistically significant effect on weight gain, food intake, food efficiency, body composition, plasma glycerol, insulin, or glucose, or on basal rectal temperatures in either diet group; there was a tendency toward increased adiposity in sympathectomized rats. Despite 95-98% depletion of NE in interscapular brown adipose tissue (IBAT), sympathectomy affected only the percentage of multilocular cells that was decreased 46-69%. Rats from small litters in both treatment groups (S and G) became obese without increased food intake (increased food efficiency), had heavier IBAT pads with bigger cells and more lipid, and were also hyperlipidemic, hyperinsulinemic, and hyperglycemic compared with controls. Therefore neonatal sympathectomy was not as significant in the subsequent development of DIO as were diet and litter size.
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PMID:Dietary obesity and neonatal sympathectomy. I. Effects on body composition and brown adipose. 639 Dec 10

Lipogenesis from U(14C) lactate was studied in hepatocytes isolated from obese Zucker rats (fa/fa) their lean littermates (Fa/?) and Sprague Dawley rats. The distribution of radioactive carbon between the glycerol and the fatty acid moieties of the acylglycerols were studied. Radioactive lactate was better utilized for glycerol formation than it was for fatty acid formation in the obese rats. However, when oleate was added to the hepatocytic incubation medium, radioactive lactate was preferentially incorporated into the fatty acid moiety of the acylglycerols. Zucker obesity classified as a "metabolic obesity" by Meyer (1) depends upon abnormalities in carbohydrate metabolism associated with increased lipogenesis. This might be explained by biochemical shifts in the utilization of nutrients (2). Among the nutrients, lactate seems to be a better source of carbon than glucose for lipid synthesis (3). It has been shown that there is an increased hepatic portal blood concentration of lactate several hours after eating: about 4 mM in Wistar rats (4) and 10-15 mM in obese Zucker rats (3). We are interested in determinating the incorporation of carbon from lactate either into glycerol or into fatty acyl moieties of hepatic acylglycerols, and in determining the influence of exogenous fatty acids on acylglycerol synthesis, since a high level of circulating fatty acids in Zucker obese rats has been reported (5). Our purpose was to determine the incorporation of lactate into glycerol and fatty acyl moieties of acylglycerols, under the influence of oleate. Hepatocytes were isolated from ad libitum fed obese Zucker rats (fa/fa), their lean littermates (Fa/?) and Sprague-Dawley rats (SD). Incorporation of lactate was studied for three hours, in order to exclude short-term regulation effects and to allow oleate to be distributed into all cellular compartments.
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PMID:Lipogenesis from U14C lactate in obese Zucker rat hepatocytes. Effect of albumin-bound oleate. 647 52

Serum glycerol and NEFA content variations are examined before and after labor in obese and normal weighing women (35 subjects). Blood glycerol and NEFA are shown to increase before delivery. Glycerol values are shown to drop to normal immediately after delivery, while NEFA values diminish to a lesser extent. Statistical analysis shown that blood glycerol increase could be pregnancy-dependent in both normal weighing and obese women, but that NEFA increase could be pregnancy-dependent in normal weighing women only. Obesity increases blood glycerol and NEFA concentration considerably, thus masking the effects of pregnancy.
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PMID:[Effect of parturition on serum glycerol and non-esterified fatty acids in obese and normal weight women]. 662 36

Lean and obese Zucker rat pups were artificially fed high-fat and high-carbohydrate diets from 10-20 d of age to determine the effect of early diet composition on de novo lipogenesis and the development of obesity in the Zucker fatty rat. Amounts fed were the same as that consumed by suckling Zucker rat pups, which also were used as dam-fed controls. Lipogenic rates were measured by in vivo incorporation of tritium from 3H2O into total lipids and fatty acid and glyceride-glycerol fractions of liver, carcass and adipose tissue. Expressed on a per g tissue basis there was no difference in lipogenic rates between lean and obese pups in any tissues, even though pups accumulated a significantly higher percentage of carcass fat. High carbohydrate feeding accelerated growth and lipogenic rates in both lean and obese rats. Dam-fed pups had the lowest rates of lipogenesis and percentage of carcass fat. Thus, diet composition and method of feeding were important determinants of de novo lipogenic rates and body energy stores at this early age, but their influence was similar in lean and genetically obese animals.
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PMID:Influence of diet on de novo lipogenesis in artificially-fed 15- and 20-day-old Zucker fatty rats. 670 56

Intravenous glucose tolerance tests were performed in 33 obese and 12 nonobese children. In addition to the glucose disappearance rate the changes in response to the glucose load in plasma insulin, FFA, glycerol, cholesterol, triglyceride, lactate and pyruvate were examined. The relationship between biochemical parameters and the glucose disappearance rate was also studied. 1. Reduced glucose tolerance, basal and glucose-induced hyperinsulinaemia were frequent in the obese children. 2. Normal or reduced glucose tolerance in spite of the apparent hyperinsulinaemia and the negative correlation between fasting insulin level and KG in the nonhypertriglyceridaemic obese group was the marker of insulin resistance in overweight children. 3. The reduced elevation of FFA in the 2nd hour of the intravenous glucose tolerance test might be the sign of an impaired lipolysis in obesity. 4. The significant negative correlation found between KG, fasting FFA and triglyceride levels in certain obese subgroups suggested the importance of FFA and triglyceride in the regulation of peripheral glucose utilization.
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PMID:Intravenous glucose tolerance test in childhood obesity: metabolite levels and their relation to glucose utilization rate (KG). 675 63

The metabolic and hormonal effects of glucagon infusion (6 micrograms/kg/h) for three hours were studied in obese children. Glucagon caused a sustained hyperglycaemia and hyperinsulinaemia and a lower than normal (non-obese) growth hormone response. Plasma triglycerides, cholesterol, glycerol and the majority of the free amino acids showed a significant decrease in comparison with the controls, while free fatty acids showed a moderate decrease. Glucagon administration revealed some hormonal and metabolic abnormalities of obesity. The effect of glucagon-induced insulin secretion and the action of pharmacologic doses of glucagon have, however, to be considered in the interpretation of the metabolic effect of glucagon.
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PMID:Effect of glucagon infusion on some plasma metabolites and hormones in obese children. 675 64

The rates of fatty acid synthesis and syntheses of other lipids were measured in vivo by determining 3H-incorporation from tritiated water or 14C-incorporation from [U-14C]glucose into white adipose tissues (WAT), brown adipose tissue (BAT) and liver, during electrical stimulation of the ventromedial hypothalamic nucleus (VMH) and the lateral hypothalamic nucleus (LH) of female rats. Electrical stimulation of the VMH markedly increased the rate of fatty acid synthesis and the conversion of glucose to total lipids, glyceride glycerol and phospholipids in interscapular BAT, but not in parametrial or retroperitoneal WAT. Conversely, on VMH stimulation, the syntheses of total lipids, glyceride glycerol and phospholipids from glucose in the liver decreased slightly, though not significantly. Electrical stimulation of the LH had no such effect. Administration of insulin increased the rate of fatty acid synthesis in both brown and white adipose tissues and in the liver. The rate of disappearance of [14C]glucose and the concentration of insulin in the blood were not changed significantly by stimulation of the VMH. These data indicate that electrical stimulation of the VMH, but not the LH, enhances lipogenesis in BAT preferentially through a mechanism not involving insulin, but probably through activation of sympathetic innervation of BAT. The physiological significance of the findings is discussed in relation to hypothalamic function in controlling non-shivering thermogenesis and obesity.
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PMID:Hypothalamic regulation of lipid metabolism in the rat: effect of hypothalamic stimulation on lipogenesis. 675 6

Lipogenesis and insulin sensitivity are evaluated in adipose tissue, liver, and diaphragm of ob/ob and non-ob/ob mice. In ob/ob mice, hepatic fatty acid synthesis from [U-14C]glucose is elevated by 4 wk of age, and adipose tissue fatty acid synthesis increases at approximately 7 wk. Hepatic activities in ob/ob mice of glucose-6-phosphate dehydrogenase (EC 1.1.1.49), 6-phosphogluconate dehydrogenase (EC 1.1.1.44), malate dehydrogenase (EC 1.1.1.40), and alpha-glycerophosphate dehydrogenase (EC 1.1.1.8) are dramatically increased by 7 wk of age. Diminished insulin-stimulated glycogen synthesis is first noted in the diaphragm of ob/ob mice at 7 wk of age. Insulin-stimulated glycogen synthesis in adipose tissue of ob/ob mice is impaired at 3 wk. At 7 wk, insulin-stimulated fatty acid synthesis in adipose tissue of ob/ob mice is markedly increased. Adipose tissue glyceride-glycerol synthesis continues to increase throughout development, whereas fatty acid synthesis decreases after 7 wk. The data suggest that alterations in lipid synthesis occur very early in the development of ob/ob mouse, prior to expression to overt obesity, at which time a major contribution to lipogenesis is made by the liver. The altered de novo lipogenesis does not precede the reported diminution in energy metabolism.
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PMID:Development of lipogenesis and insulin sensitivity in tissues of the ob/ob mouse. 678 59

Adipose tissue slices were prepared from middle subcutaneous or perirenal adipose tissue excised from pigs of different ages (and obesity) and incubated with [U-14C]glucose. After incubation, the slices were fixed with osmium tetroxide and separated into diameter ranges of 20--63, 63--102, and 102--153 microgram, respectively. Following determination of cell size and number, the fixed adipocytes were decolorized with H2O2 prior to quantification of glucose conversion to total lipid, glyceride fatty acids, glycerideglycerol, and CO2. Glucose conversion to total lipid or CO2 was unaffected by the presence of purified porcine insulin (0, 10, 100, 1000, and 100,000 microM/ml). Within animals, adipocytes of different sizes were not different with regard to insulin sensitivity. Within a weight (age) group, conversion of glucose to total lipid (insulin present) or to glyceride fatty acids and glyceride-glycerol (insulin absent) per cell was significantly greater in large adipocytes compared to small adipocytes, regardless of the group examined. With increasing weight or age, there was a markedly decreased conversion of glucose to total lipid and glyceride fatty acids among adipocytes of similar size within a cell-size fraction. The diminution in glucose metabolism was greater (as a percentage) in 20--63 microgram adipocytes than for 63--102 or 102--153 microgram adipocytes. However, for all cell-size fractions there was a marked decrease in glucose conversion to fatty acids. Glyceride-glycerol synthesis was impaired in adipocytes from older pigs, but the decrease was less than observed for glyceride fatty acid synthesis.
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PMID:Effects of cell size and animal age on glucose metabolism in pig adipose tissue. 678 14


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