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

Atherosclerosis, the most frequent complication of diabetes, could be the result of hyperlipidemia, among other factors. Mounting evidence suggests that reducing the concentration of triglyceride-rich lipoprotein, which influences the production of the possibly atherogenic intermediate density lipoprotein (IDL), might diminish the circulating level of potentially atherogenic lipoproteins. Hypertriglyceridemia, even in the absence of obesity, is associated with insulin resistance. To compensate, pancreatic B cells respond to glucose challenge by producing hyperinsulinemia. If the B cells cannot respond adequately, carbohydrate intolerance ensues. Insulin-treated diabetics may also become hyperinsulinemic because routine insulin injection may not reflect physiologic need and because the insulin is administered peripherally rather than portally. Hyperinsulinemia increases the production of circulating triglyceride. It appears to do this in rats by causing the production of more triglyceride-rich lipoprotein particles rather than by increasing the triglyceride content of each particle. Further, at least in rats, the insulin-induced increase in triglyceride production requires the presence of supplementary dietary fructose. Hyperinsulinemia also increases the activity of adipose tissue lipoprotein lipase and the degradation of very low density lipoprotein (VLDL). The concentration of VLDL depends on balance of production and degradation. Accelerated VLDL degradation leads to an increase in IDL production. Because there is mounting evidence that IDL may be atherogenic, this cycle could accelerate atherogenesis. As such, it is reasonable to postulate that reducing the concentration of triglyceride-rich lipoproteins would break this cycle and would diminish the circulating level of potentially atherogenic lipoproteins.
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PMID:Hypertriglyceridemia and carbohydrate intolerance: interrelations and therapeutic implications. 352 Dec 48

To evaluate mechanisms of diabetes-induced changes in very-low-density lipoprotein (VLDL), VLDL triglyceride (TG) and VLDL apolipoprotein B (apoB) metabolism were studied in 12 obese Pima Indian control subjects and in 15 Pima Indian obese non-insulin-dependent diabetics. Eleven of the diabetics were restudied after reduction of hyperglycemia with oral sulfonylurea therapy. In addition, adipose, muscle, and postheparin lipoprotein lipase and postheparin hepatic lipase activities were measured in all subjects. Obese diabetics as compared with obese controls showed a trend toward increased production of VLDL TG (46 +/- 4 vs. 35 +/- 6 g/day, P = .10) but not of VLDL apoB (1595 +/- 106 vs. 1597 +/- 164 mg/day, NS); production of VLDL TG declined to control levels (33 +/- 4 g/day, P less than .05) during therapy, whereas there was no change in production of VLDL apoB. Diabetics had a clearance defect for VLDL, indicated by significantly lower fractional catabolic rates for both VLDL TG (10.6 +/- .9 vs. 13.1 +/- .9 pools/day, P less than .05) and VLDL apoB (5.6 +/- .4 vs. 7.5 +/- 0.7, P less than .05) as compared with controls; fractional catabolic rates increased after therapy (to 13.3 +/- 1.5, P less than .05, and 6.7 +/- .4, P less than .05, respectively). In the diabetics, this decrease in clearance was accompanied by a lower adipose lipoprotein lipase (.30 +/- .09 vs. .92 +/- .25 mumol X g-1 X h-1, P less than .01), which increased during therapy (to .61 +/- .17, P less than .05). Hepatic lipase also decreased significantly after therapy (27.4 +/- 3.6 to 26.4 +/- 3.2, P less than .01). Composition of VLDL in diabetics was also abnormal, indicated by a higher TG/apoB ratio (14.7 +/- .6 vs. 11.7 +/- .8, P less than .01); this ratio fell during therapy (to 12.5 +/- .8, P less than .05). The data indicate there are multiple abnormalities in structure and metabolism of VLDL in non-insulin-dependent diabetics. Control of hyperglycemia with sulfonylureas has the capability of reversing some of these abnormalities.
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PMID:Effects of NIDDM on very-low-density lipoprotein triglyceride and apolipoprotein B metabolism. Studies before and after sulfonylurea therapy. 353 Aug 55

Adrenalectomy has been shown to reduce the development of obesity in adult Zucker fatty rat. In this study, we examined whether adrenalectomy could prevent the emergence of obesity and correct any of the first abnormalities to develop in fa/fa pups. Four-day-old Zucker pups were adrenalectomized and fed by adrenalectomized wet nurses until 11 days of age. The frequency distribution curves of fat cell volume clustered in two groups as they do in control litters, providing evidence that two phenotypes were present. Oxygen consumption measured at 8 days of age was significantly lower in fa/fa than in Fa/fa. Adrenalectomy did not restore the decreased oxygen consumption of fa/fa. In control litters, the GDP binding to brown adipose tissue mitochondria was twofold lower, whereas fatty acid synthase activity of this tissue was significantly increased in fa/fa pups. In inguinal adipose tissue of fa/fa pups, fatty acid synthase, and lipoprotein lipase activities were twice as active as in the tissue of lean pups. In adrenalectomized fa/fa pups, none of these metabolic abnormalities was corrected. The results demonstrate that adrenalectomy early in life did not prevent the emergence of obesity in suckling fa/fa rats.
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PMID:Deprivation of corticosterone does not prevent onset of obesity in Zucker fa/fa pups. 355 27

Adipose tissue distribution is an important predictor of obesity-associated morbidity and mortality. A central ('male') fat distribution is associated with increases in intra-abdominal adipose tissue which might be of metabolic importance. Although many recent studies have pointed out significant regional differences in the size and metabolism of subcutaneous fat cells intra-abdominal depots have not been systematically examined. We compared fat cell sizes (FCS) and lipoprotein lipase activity (LPLA) of two internal (omental, mesenteric) and four subcutaneous (SQ) sites (femoral, gluteal, abdominal, epigastric) in morbidly obese patients (26 premenopausal women and 14 men). Men had larger internal FCS than women while women had larger SQ FCS in the gluteal and femoral depots. Mesenteric FCS were largest of all sites in men. In women, omental fat cells were the smallest of all sites sampled but omental fat cells were as large as SQ sites in men. A more central distribution of fat in women (high waist/hip ratio) was associated with large mesenteric fat cells. Calculation of total fat cell number based on SQ FCS only, revealed sex differences that were eliminated by also using intra-abdominal FCS in the calculation. Averaged across all six sites, women had higher LPLA than men. Higher LPL activities were found in the lower-body subcutaneous sites with enlarged fat cells in women. However, the relative enlargement of intra-abdominal FCS in men was not associated with increased LPLA. In conclusion, sex- and site-specific variations in the distribution of FCS and LPLA in internal and SQ fat depots emphasize the importance of analyzing these depots in studies of fat cell number and adipose tissue metabolism.
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PMID:Sex differences in regional distribution of fat cell size and lipoprotein lipase activity in morbidly obese patients. 361 Apr 66

Lack of movement is an essential cause for the development of obesity and dys- and hyperlipoproteinaemias. These disturbances of metabolism are risk factors for the development of the early coronary heart disease. The medicamentous treatment of these diseases can be decisively supported by dosed application of athletic exercises (sports therapy). Persevering athletic exercises of at least 30 min duration increase the activity of lipocatabolic enzymes (lipoprotein lipase, serum-lecithin-cholesterol-acyl transferase). As measure of exercise in sports therapy perseverance-orientated kinds of sport of altogether 2 hours a week are recommended.
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PMID:[Sports therapy in obesity and lipid metabolism disorders]. 363 Feb 94

Obesity in humans is associated with decreased plasma levels of high density lipoprotein (HDL), but the mechanisms effecting this relationship have not been established. Four treatment groups were used to develop a range of moderate adiposity: rat pups were raised in litters of 4 or 14 and fed from weaning diets of 6 or 24% fat (wt/wt) for 15-17 wk. Lipoproteins from plasma and from a recirculating in situ liver perfusion system were then separated and analyzed, lipoprotein lipase (LPL) activity was assayed in samples of adipose tissue and skeletal muscle and body composition and cholesterol concentrations of various tissues were determined. There was little effect of the diet or litter size treatments on plasma lipids or lipoprotein profiles. Compared to the marked changes in lipid and lipoprotein metabolism that have been observed in severely obese animal models, there was generally little effect of the treatments used to produce this model of moderate diet-induced adiposity. Adiposity was unrelated to plasma total cholesterol and triglycerides. While fatness was positively, although weakly, correlated with plasma levels of several HDL components, including HDL cholesterol, there were no consistent treatment effects on these measures. Plasma HDL levels and adiposity were unrelated to hepatic HDL production or tissue LPL activities. A review of the literature suggests that differences in plasma HDL responses to adiposity in humans and in experimental animals may be due to inherent species differences in lipoprotein metabolism.
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PMID:Lipoprotein metabolism in a rat model of diet-induced adiposity. 366 78

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

The activity of lipoprotein lipase (LPL) was studied in interscapilar brown adipose tissue (BAT), epididymal white adipose tissue (WAT) and in the heart of lean and obese adult Zucker rats maintained at 22 degrees C or adapted to cold (10 degrees C). In WAT the specific activity per gram of tissue was lower in obese than in lean rats but the total activity within the tissue was three-fold higher. Cold acclimation did not modify total activity in either lean or obese rats. In BAT, but not in the heart, both specific and total activities were lower in obese than in lean animals. They were enhanced in both tissues following cold acclimation. Six-hour fasting led to a decrease in specific activity in WAT of lean rats but had no effect in obese animals; an increase was observed in BAT and heart of both genotypes. Insulin administration has no effect on activities in WAT in either 22 or 10 degrees C adapted obese rats. Norepinephrine administration stimulates LPL activity in BAT and heart of all groups. It is concluded that the lack of development of obesity previously observed in obese rats following cold acclimation is not due to a decreased capacity of lipid uptake by WAT. It might in part be due to an increased lipid oxidation in BAT.
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PMID:Effects of cold acclimation on the activity of lipoprotein lipase in adipose tissues of genetically obese Zucker rats. 389 31

Temporal and spatial patterns of lipid deposition, vascularization and collagen deposition were described for subcutaneous adipose tissue in the fetal pig. Enzyme cytochemical changes were reported as they relate to the morphological differentiation of the subcutaneous depot. There are distinct temporal lags between the appearance of specific enzymes in adipocytes. For example, NADH-tetrazolium reductase activity appeared earliest whereas esterase activity appeared before lipoprotein lipase (LPL) activity. Adipose tissue primordia has been localized around specific tissue components in rat and pig tissues. These tissue components include hair follicles, sweat glands, large nerves, large blood vessels and mammary gland ducts. Lipid and enzyme cytochemistry demonstrates physical continuity between primordial cells and differentiated fat cell clusters. Alterations in maternal and/or fetal endocrine or metabolic profiles result in specific changes in fetal subcutaneous adipocytes. For example, maternal diabetes significantly increases cell size whereas genetic obesity has little effect on cell size but increases cellular LPL activity significantly. A comparison of subcutaneous and perirenal depots in the pig fetus indicated several depot specific anatomical and enzyme histochemical traits. Blood vessel architecture and vascular alkaline phosphatase activity clearly demarcated perirenal and subcutaneous depots in the fetus. These data indicate that site to site variations of adipose tissue characteristics may be reflecting intrinsic stromal-vascular aspects of specific locations.
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PMID:Anatomical and enzyme histochemical differentiation of adipose tissue. 393 90

Rats were overfed during the suckling period by litter size manipulation in order to investigate the possible contribution of preadipocytes from the stroma-vascular compartment of adipose tissue to the development of obesity. Rats raised in litters of four pups were overfed; for normal feeding we assigned eight pups per litter. As early as 10 d of age, overfed rats became fatter than controls, and showed an increase in both plasma insulin and triacylglycerol levels. At this age, adipose tissue overdevelopment arose only from adipocyte hypertrophy, since hyperplasia occurred only at 15 d of age. Concurrently, compared to normal feeding, overfeeding led to significantly higher activities of lipoprotein lipase (LPL), glycerophosphate dehydrogenase (GPDH) and glycerophosphate acyltransferase (GPAT) in mature fat cells; 10-d-old overfed pups exhibited a higher stromal cell number. Further separation of this heterogeneous fraction by density gradient centrifugation showed a higher preadipocyte number as compared to that of controls. In stromal cells, LPL, GPDH, GPAT and acyl CoA ligase activities were detected during the suckling period. As compared to controls, overfeeding induced an increase in both LPL and GPDH activities in 10-d-old pups. Results indicate that overfeeding in early life induced an excess of fat storage capacity through a simultaneous increase in proliferation and differentiation rates of adipocyte precursors.
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PMID:Role of adipocyte precursors in the onset of obesity induced by overfeeding in suckling rats. 395


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