Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lipoprotein lipase (LPL) enzyme activity in epididymal adipose tissue from obese and lean Zucker rats was measured. At 5, 10, 13, and 20 wk of age obese rats have heavier fat pads, larger fat cells, and more LPL per epididymal fat pad and per fat cell than do their lean littermate controls. Although LPL per fat cell increased as fat cell size increased in lean rats, the increased LPL activity in the obese could not be attributed solely to increased fat cell size. When obese and lean rats had similar cell sizes, LPL per fat cell was still significantly increased in the obese compared to lean. Furthermore LPL activity was increased in "preobese" (fa/fa) rats compared to either lean genotype (Fa/fa or Fa/Fa) during the second postnatal week. The data suggest that early increments in LPL activity in adipose tissue of the "pre-obese" rat may significantly contribute to the early fat cell hypertrophy seen during the development of this genetic obesity. Furthermore, early increased LPL activity may prove useful as a predictor of the onset of obesity.
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PMID:Increased adipose tissue lipoprotein lipase activity during the development of the genetically obese rat (fa/fa). 72 44

Oxidation in vivo of [14C]triolein to 14CO2 was significantly lower in obese (fa/fa) Zucker rats as compared with their lean (+/?) controls. In response to a 24 h starvation period, both lean and obese rats showed an enhanced rate of [14C]triolein oxidation. There were, however, no changes in the rate of intestinal absorption of [14C]triolein between the lean and obese animals. Conversely, the total tissular [14C]lipid accumulation was significantly higher in white adipose tissue, carcass and plasma in the obese animals, whereas that of brown adipose tissue was lower. This was associated with a marked hyperinsulinaemia and hypertriglyceridaemia in the fa/fa animals. Starvation dramatically decreased [14C]lipid accumulation in white adipose tissue of the lean Zucker rats, but had no effect in the obese rats. The lipogenic rate of the obese rats was significantly higher than that of lean rats in liver, white adipose tissue, skeletal muscle and carcass. Lipoprotein lipase activity (per g of tissue) was significantly lower in both white and brown adipose tissue of obese versus lean rats; however, total activity was higher in both tissues. Starvation significantly lowered perigenital-adipose-tissue lipoprotein lipase activity in the lean groups, and had no effect in the obese ones. These results demonstrate that the tissue capacity of exogenous lipid uptake is involved, but cannot be the only factor influencing the maintenance of obesity in these animals. Thus, in the adult fa/fa rat, the large increase in obesity is not solely dependent on a deviation of energy-producing substrate metabolism towards the storage of lipids in white fat. Other factors, such as a low rate of oxidation, a high lipogenic rate and decreased brown-adipose-tissue activity are involved in the perseverance of the obesity syndrome.
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PMID:Lipid metabolism in the obese Zucker rat. Disposal of an oral [14C]triolein load and lipoprotein lipase activity. 201 94

Lipoprotein lipase is an important regulator of lipid and lipoprotein metabolism. It also contributes to the lipid and energy metabolism of different tissues in varying ways. Although the synthesis, manner of secretion, and mechanism of endothelial binding of lipoprotein lipase appear similar in all tissues, the factors that control gene expression and posttranslational events related to processing vary from tissue to tissue. The actual molecular events that determine this tissue specificity are not yet understood. In the future, however, it may be possible to stimulate or inhibit the activity of lipoprotein lipase in specific tissues and to alter metabolic processes so as to improve the quality and length of life in patients with metabolic diseases such as hypertriglyceridemia, HDL2 deficiency, and obesity.
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PMID:Lipoprotein lipase. A multifunctional enzyme relevant to common metabolic diseases. 230 Jan 16

Bilateral basomedial hypothalamic (BMH) electrolytic lesions in White Leghorn cockerels produced six main physiological categories characterized by typical sets of symptoms: 1) functional castration (FC); hyperphagia, obesity, occasional diabetes insipidus, involuted adenohypophysis, dwarfism, atrophied comb and testes, reduced hematocrit, reduced plasma testosterone and thyroid activity, involuted thymus and adrenal cortex and elevated liver fat and plasma triglycerides and free fatty acids. The FC birds demonstrated defective immune response for the first 12 to 16 wk post-surgery. 2) functional castration with large comb (FCLC); hyperphagia, obesity, transient diabetes insipidus, slight diminution of adenohypophy-seal weight with marked reduction in basophilic cell population, fully atrophied testes but only slight reduction in comb size and hematocrit, plasma testosterone levels between those found in the first category and the control. 3) obese with normal testes (ONT); hyperphagia, obesity, high level of plasma lipids, normal histological organization of the adenohypophysis, normal testes, semen production and comb size. The next three categories exhibited physiological syndromes identical to the former three categories except for food intake, which operationally could be defined as normal. A marked difference among the BMH-lesioned birds was found in sexual behavior when the FC birds completely lost their libido. None of the replacement therapy regimens caused complete rehabilitation from adiposity or restoration of reproductive traits. Lipoprotein lipase activity increased at an early stage postlesioning and preceeded the development of hyperphagia. Placement of BMH lesions in newly hatched chicks resulted in marked dwarfism and obesity without hyperphagia. The BMH-lesioned heavy breed White Rock cockerels exhibited a lesser degree of adiposity than the light White Leghorn birds. Removal of the olfactory bulbs and destruction of the septal area resulted in increased thyroid activity, with secondary hyperphagia without obesity. In a short-term study, administration of sodium pentobarbital to the BMH area resulted in increased feeding. Conversely, glucose administration to the same area suppressed feeding in satiated but not in food-deprived chickens.
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PMID:Role of the basomedial hypothalamus in regulation of adiposity, food intake, and reproductive traits in the domestic fowl. 267 24

We measured serum lipids, lipoproteins and post-heparin plasma lipases, lipoprotein lipase and hepatic lipase, in 12 female patients with Type 1 (insulin-dependent) diabetes (postglucagon C-peptide undetectable), in 11 female insulin-treated patients with Type 2 (non-insulin-dependent) diabetes (postglucagon C-peptide greater than 0.60 nmol/l) and in 16 non-diabetic female control subjects. These three groups of subjects were similar with respect to age and obesity. Insulin dose was similar in patients with Type 1 and with Type 2 diabetes. HDL and HDL2 cholesterol were lower in patients with Type 2 diabetes than in non-diabetic control subjects (p less than 0.05) but did not differ between patients with Type 1 diabetes and non-diabetic control subjects. No difference in lipoprotein lipase activity was seen between the groups. The highest levels of lipoprotein lipase and hepatic lipase activities were observed in patients with Type 2 diabetes. Lipoprotein lipase activity correlated significantly with HDL cholesterol in patients with Type 1 diabetes (p less than 0.01) and in patients with Type 2 diabetes (p less than 0.001) but not in control subjects. Hepatic lipase activity did not correlate significantly with HDL cholesterol in any of the groups. In conclusion, postheparin plasma lipoprotein lipase and hepatic lipase activities do not seem to explain the difference in HDL cholesterol concentration between patients with Type 1 and Type 2 diabetes.
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PMID:Relationship between postheparin plasma lipases and high-density lipoprotein cholesterol in different types of diabetes. 342 2

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

We report on clinical and metabolic studies of a newly delineated lipomatosis, characterised by an abnormal mediastinal and abdominal accumulation of fat, without obesity. The clinical features, which occurred in all the patients studied, are: Exertional dyspnoea due to a space-occupying mediastinal accumulation of fat, without evidence of cardiac or pulmonary disease. A pseudo-ascitic abdominal enlargement, due to intra- and retroperitoneal accumulation of fatty tissue. Insulin-independent diabetes mellitus. Type IV hyperlipidaemia and elevated levels of plasma uric acid were observed in four patients. Intra-abdominal lipomatous tissue, obtained during laparoscopy from four patients, demonstrated a reduced lipolytic response to beta-adrenergic stimulation. Thus, fat deposition in the abdominal and mediastinal areas could be causally related to defective lipid mobilization in lipomatocytes. Lipoprotein lipase activity in abdominal adipose tissue were normal in two patients (10.0 and 10.6 nmol/g/min) and markedly elevated in another two patients (37.3 and 49.9 nmol/g/min), as compared with controls (12.7 +/- 2.1 nmol/g/min). When expressed on per cell basis, LPL activity in lipomatous tissue was significantly higher than in control tissue (3.21 +/- 1.1 nmol/10(5) cell/min vs 0.92 +/- 0.16 nmol/10(5) cell/min). Lipoprotein fractionation did not demonstrate consistent modification of the serum lipoprotein pattern. HDL and HDL2 cholesterol values were reduced, even in patients with elevated LPL activity in adipose tissue.
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PMID:Mediastino-abdominal lipomatosis: deep accumulation of fat mimicking a respiratory disease and ascites. Clinical aspects and metabolic studies in vitro. 651 1

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

(1.) Male and female rats reared in litters of four gained body weight more rapidly than animals reared in litters of 16. The differences were more marked in males than females and became less marked in both sexes with advancing age. (2.) The relative weights of the perigenital, perirenal, subcutaneous and intramuscular white-adipose-tissue sites in the animals from small litters indicated their relative obesity compared with animals from large litters. A sex-related difference in the distribution of adipose tissue between the four sites was seen in animals reared in litters of both four and 16. (3.) Although at 30 days of age all the animals had more numerous and larger fat-cells in their white-adipose-tissue depots than animals reared in large litters, the pattern of change thereafter was both site- and sex-specific. During the post-weaning period (30-300 days), although detailed differences were apparent between sites, a general pattern of increased cell size in males and increased cell numbers in females emerged as being the important determinants responsible for the differences in depot sizes seen when animals from litters of four and 16 were compared. (4.) Lipoprotein lipase activities, expressed as units/g fresh wt. of tissue, in the depots of animals reared in groups of four were unaltered compared with those reared in groups of sixteen during the post-weaning period (47-300 days of age), and enzyme activities expressed per depot merely reflected differences in tissue weights. (5.) Lipoprotein lipase activities per 10(6) cells were higher in males reared in fours compared with those reared in sixteens of equivalent age, but were unaltered for females. (6.) The persistent hyperinsulinaemia of animals reared in litters of four is discussed in relation to the observed differences in enzyme activity and white-adipose-tissue cellularity.
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PMID:The development of white adipose tissue. Effect of litter size on the lipoprotein lipase activity of four adipose-tissue depots, serum immunoreactive insulin and tissue cellularity during the first year of life in male and female rats. 699 14

Polygenic obese (M16) and nonobese (ICR) mice were fed ad libitum either a high-fat (FAT) or high-carbohydrate (CHO) diet from 6 to 10 weeks of age. After this four-week period, M16 exceeded (P less than 0.01) ICR mice and FAT-fed exceeded (P less than 0.01) CHO-fed mice in body energy percent, body fat percent, and weight and proportional weight of epididymal and subcutaneous fat pads. Fat cell size and number in both fat depots were greater (P less than 0.01) in the M16 than in the ICR line. Mice fed FAT had larger (P less than 0.01) fat cells in both depots compared with CHO-fed mice, but fat cell nuber was not altered significantly. M16 mice were hyperglycemic, hyperinsulinemic and hypercholesterolemic, Dietary treatment did not affect glucose or insulin levels, but cholesterol was greater (P less than 0.01) on FAT than on CHO diet. Lipoprotein lipase and fatty acid synthetase activities were greater in M16 than in ICR mice, while fatty acid synthetase activity was greater in mice fed CHO than in those fed FAT. Genotype by diet interactions were not important for the traits studied. Polygenic obese mice, developed by selection for increased growth rate, share many of the characteristics of the single gene obesity syndromes in rodents. The development of obesity in polygenic obese mice may be due, in part, to an acceleration of the normal developmental process of growth, in addition to hyperphagia and increased energetic efficiency.
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PMID:Adipose cellularity, serum glucose, insulin and cholesterol in polygenic obese mice fed high-fat or high-carbohydrate diets. 703 Aug 75


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