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

The effects of estradiol and progesterone on food intake, body weight, carcass adiposity, and adipose tissue lipoprotein lipase (LPL) activity were investigated in weanling female rats. Treatment with estradiol benzoate (EB) reduced body weight gain in ovariectomized (OVX) weanlings as it does in adults. However, other responses to EB were attenuated or absent in weanlings. EB treatment did not reduce food intake, carcass adiposity, or adipose tissue LPL activity. This impaired responsiveness to EB may be due to decreased levels of cytoplasmic estrogen receptors in liver and adipose tissue (but not hypothalamus) in weanlings. On the other hand, responsiveness to progesterone was adultlike in weanlings. Treatment of OVX, EB-primed weanlings with progesterone increased food intake, body weight gain, and carcass adiposity. This adultlike responsiveness to progesterone was associated with adultlike levels of adipose tissue progestin receptors. However, progesterone treatment did not increase adipose tissue LPL activity in weanlings, indicating that changes in LPL activity are not necessary for progesterone-induced obesity.
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PMID:Effects of estradiol and progesterone on food intake, body weight, and carcass adiposity in weanling rats. 723 6

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

Activity of lipoprotein lipase (LPL) was determined in whole adipose tissue and isolated adipocytes, and in heart and skeletal muscle that contained predominantly red or white fiber types in lean and obese Zucker rats. In rats of both sexes at 9-11 and 26-30 wk of age, no differences were observed between lean and obese rats when LPL activity of the perirenal (PR), subcutaneous (SC), and mesenteric (M) adipose tissues was expressed per millimole of tissue triglyceride. Within each sex, data relating the LPL content of isolated adipocytes to cell size was a linear function in which data for lean and obese rats fell on the same regression line. Measurement of the distribution of adipose tissue LPL activity between adipocytes and other tissue constituents showed no differences between lean and obese rats, a finding that is inconsistent with the hypothesis that obesity results in part by an alteration in adipose tissue enzyme distribution. Activity of LPL in the myocardium and red fiber types in the younger group of both sexes showed significant decreases in obese animals. This was also true for white fibers of males but not females. No differences in heart or muscle LPL between lean and obese rats were observed in the older group of either sex.
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PMID:Lipoprotein lipase activities in adipose tissues and muscle in the obese Zucker rat. 727 Jun 78

Obesity is detectable in adult male Wistar rats three weeks after initiation of a high-fat diet. Although there was an immediate increase in muscle lipoprotein lipase (LPL) activity, and a progressive adaptative response in adipose tissue leading to inhibition of de-novo lipogenesis, loss of insulin sensitivity and decreased functional LPL activity, the ensuing reorientation of lipid metabolism failed to prevent obesity. It is concluded that there is no fixed relationship between enlargement of adipose tissue and LPL activity in this tissue, at onset of obesity.
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PMID:Lipoprotein lipase at onset of obesity induced in rats by a high-fat diet. 731 88

Adipose tissue fat cell size and lipoprotein lipase (LPL) activity were determined in the retroperitoneal and subscapular depots of nonpregnant, pregnant, and postpartum rats fed either a standard laboratory diet or a high-fat diet containing 55% fat by weight. High-fat feeding for 20 days increased, in nonpregnant rats, fat cell size and LPL activity two- to threefold in both depots. In pregnant rats at term, fat cell size was increased and LPL activity was depressed in both dietary groups. Twenty days postpartum, both retroperitoneal fat cell size and LPL activity were decreased in proportion to the size of the litter. Rats not allowed to lactate had fat cell sizes and LPL activity that were not significantly different than in nonpregnant controls. Fat cell size and LPL activity in rats nursing four pups were reduced to 77% and 36% of control, respectively. Those nursing a normal-sized litter of eight pups demonstrated a further reduction of fat cell size to 38% and of LPL activity to 2% of nonpregnant control values. High-fat feeding and obesity did not prevent the fat loss and decreased LPL activity associated with lactation; fat cell size was decreased to 61% and LPL activity to 3% of control values. Values for the subscapular depot followed essentially the same pattern as that observed for the retroperitoneal depot. Mammary LPL activity was increased more than tenfold in animals nursing four or eight pups compared with values at term, whereas no activity was detected in rats not allowed to lactate.
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PMID:Diet, pregnancy, and lactation: effects on adipose tissue, lipoprotein lipase, and fat cell size. 741 58

Twenty-three apparently normal untrained men aged 20--55 participated in a 4-month self-regulated training programme ending in a marathon run. Fasting plasma and lipoprotein lipid concentrations, adipose tissue lipoprotein lipase activity, anthropometric data, alcohol consumption, smoking habits, weekly mileage run and performance on a bicycle ergometer were recorded before and after the training period. Training induced an increase in high density lipoprotein cholesterol (HDL-C) concentration which was not directly related to concomitant decreases in mean very low density lipoprotein cholesterol (VLDL-C) concentration or mean total skinfold thickness. The degree of the changes in VLDL lipids and HDL-C levels were related to pretraining values, and changes in HDL-C and VLDL triglycerides (VLDL-TG) were also associated. Initial total skinfold thickness correlated inversely with the change in VLDL-TG levels during training. The pretaining concentration of VLDL-C was related to the corresponding value for HDL-C after training. The magnitude of exercise-induced changes in VLDL-C and HDL-C levels are more related to pre-training levels than to changes in measured exercise parameters, indices of obesity or adipose tissue lipoprotein lipase activity. However, the level of adiposity of subjects at the beginning of the study influenced the response of VLDL-TG levels to increased physical activity. The data suggest that VLDL contributes to the increase in HDL-C levels with exercise but is not the major source of the increment.
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PMID:Physical activity and plasma lipoprotein lipid concentrations in men. 742 1

Adipose tissue lipoprotein lipase (ATLPL) is responsible for the provision of lipoprotein-derived fatty acids to adipocytes for storage as triglycerides. Fasting ATLPL has been shown to be decreased in non-insulin-dependent diabetes mellitus (NIDDM), an insulin-resistant state. Medically uncomplicated obesity, another state of relative insulin resistance, is associated with decreased stimulation of the enzyme in response to metabolic stimuli. It was therefore hypothesized that the increased insulin resistance of NIDDM would result in an even greater defect in the response of ATLPL to insulin/glucose. Gluteal adipose tissue biopsies were performed in 13 premenopausal obese women with NIDDM, before and after 6 hours of intravenous insulin and glucose. Metabolic data from these studies were then compared with those obtained from 26 nondiabetic obese women of similar age, weight, and fasting insulin concentration (obese controls [OBC]). As expected, fasting gluteal ATLPL activity was lower in the NIDDM group than in OBC (3.7 +/- 0.9 v 11.1 +/- 1.6 nmol free fatty acids [FFA]/min/10(6) cells, P = .0003). The change in ATLPL activity (delta ATLPL) in response to a 6-hour insulin/glucose infusion was not statistically different between the two groups (2.2 +/- 1.1 v 4.7 +/- 1.2, P = .114). However, in NIDDM subjects there was a strong positive relationship between delta ATLPL and glycohemoglobin (GHb) level (r = .883, P = .0001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Glycohemoglobin levels relate to the response of adipose tissue lipoprotein lipase to insulin/glucose in obese non-insulin-dependent diabetes mellitus. 747 37

An elevation of lipoprotein lipase (LPL) activity in adipose tissue is considered a possible cause of obesity. However, transgenic mice that overexpress the human LPL gene showed no increase in fat deposition as compared with controls. In the present study, we investigated effects of LPL on fat accumulation. Respiratory quotients and uptake of [3H] triolein by tissues (white and brown adipose tissue, and skeletal muscles) did not differ significantly for transgenic and non-transgenic mice. The mRNA levels of hormone-sensitive lipase (HSL) and HSL activity in adipose tissue during feeding were higher in LPL transgenic mice than in controls. Results suggest that the overexpression of LPL does not induce obesity by enhancing the hydrolysis of triglycerides in adipose tissue.
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PMID:Overexpression of human lipoprotein lipase increases hormone-sensitive lipase activity in adipose tissue of mice. 759 4

This study was undertaken to determine whether administration of a thermogenic beta-agonist drug to Zucker fatty rats could correct some of the earliest metabolic defects detectable in brown adipose tissue (BAT). Fa/fa and fa/fa littermates were given oral administration of BRL-35135 from 8 to 16 days of age. In fa/fa rats, the lipid content of white and brown adipose tissues was significantly reduced. In the BAT of fa/fa rats, thermogenic capacity was restored to the level observed in Fa/fa rats, whereas hyperactivity of fatty acid synthetase was abolished, and a deficit in lipoprotein lipase (activity and mRNA) was partly corrected. Hyperinsulinemia in fa/fa pups was significantly reduced. The decreased content of GLUT-4 mRNA that characterized BAT of fa/fa pups was also restored to normal. At variance with observations in preobese rats, BRL had very little or no effect on lean Fa/fa rats. The present study reveals that chronic administration of a beta-agonist drug early in life prevents emergence of most of the metabolic abnormalities that characterize fa/fa rats at the onset of obesity. This suggests that impaired sympathetic activity may play a role in the development of this genetic obesity.
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PMID:Effect of the beta-adrenoceptor agonist BRL-35135 on development of obesity in suckling Zucker (fa/fa) rats. 761 76

Lipolytic and lipoprotein lipase (LPL) activities were studied in isolated human adipocytes obtained from two intraabdominal depots (round ligament and omental) and from the subcutaneous abdominal region of nine severely obese premenopausal women (with body mass indices ranging from 37 to 51 kg/m2), aged 36 +/- 3 yr, undergoing gastrointestinal surgery. Both fat cell weight and LPL activity were significantly greater in round ligament adipose cells than in subcutaneous abdominal or in omental adipocytes (P < 0.05). The antilipolytic effect of insulin and the sensitivity to this hormone were also higher in round ligament adipose cells than in omental adipocytes (P < 0.05). Although epinephrine initiated a similar biphasic profile of response in all cell types, the catecholamine promoted a weaker inhibition of lipolysis in omental adipocytes than in subcutaneous abdominal adipose cells (P < 0.05). In addition, a lack of regional variation was found in the maximal antilipolysis initiated by UK 14304 and the alpha 2-adrenoceptors was higher in both subcutaneous abdominal and round ligament fat cells than in omental adipocytes. Moreover, the maximal lipolytic response to isoproterenol or to agents acting at post-receptor levels was not different among fat depots. Finally, a lower beta-adrenergic lipolytic sensitivity associated with a reduced beta-adrenoceptor density was observed in round ligament as compared to omental adipose cells. These data suggest that in massively obese premenopausal women, omental and round ligament adipose tissues show distinct metabolic properties that may contribute to limit the impact of intraabdominal obesity.
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PMID:Regional variation in adipose tissue metabolism of severely obese premenopausal women. 761 15


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