Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In two patients with primary Type V hyperlipoproteinemia with typical clinical features including recurrent bouts of abdominal pain a myocardial infarction was diagnosed. In both cases coronary angiography revealed a severe three vessel disease. The case reports demonstrate that the incidence of ischemic heart disease in patients with Type V hyperlipoproteinemia is higher than reported in the literature. In each case of severe abdominal pain, even in younger Type V patients, a myocardial infarction has to be excluded, In both patients a selective depression in the activity of lipoprotein lipase was found. The possible pathogenetic implication of this finding will be discussed.
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PMID:[Coronary heart disease in patients with primary type V hyperlipoproteinemia (author's transl)]. 20 63

DELTA1-tetrahydrocannabinol (delta1-THC), a highly lipid soluble and active principle of cannabis, was injected each day (25 mg/kg) s.c. in mice from the estimated 13th day of pregnancy. Delta1-THC-treated mice showed no increase in the wet weight or DNA content of their mammary glands during the period of investigation from before parturition until the 12th day post-partum. A marked increase in mammary-gland lipoprotein lipase activity w,s found in control mice at parturition and this was suppressed by delta1-THC. Prolactin rose to a peak level in plasma earlier in lactation in the control mice than in the delta1-THC-treated mice. This delayed rise in plasma prolactin due to delta1-THC may account for the depression of mammary gland growth and development by the drug and for the delay in the appearance of high activities of lipoprotein lipase until later in lactation.
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PMID:The effects of delta1-tetrahydrocannabinol on mammary gland growth, enzyme activity and plasma prolactin levels in the mouse. 69 71

Lipoprotein lipase (LPL) activity was measured in adipose tissue, heart and diaphragm in Sprague--Dawley rats after estrogen therapy or orchiectomy. Enzyme activity was measured by incubation of tissue fragments with a triolein emulsion in the presence of serum and heparin. In confirmation of other work, depression of adipose tissue LPL followed estradiol treatment in pharmacologic or near-physiologic doses. Cardiac and diaphragmatic muscle LPL were increased. Estrogen-treated male animals showed growth retardation. However, they gained weight steadily and did not show significant differences in serum insulin, glucose of D-beta-hydroxybutyrate. The effects of estradiol in male animals were reversed by sequential fasting and re-feeding. At times during growth and aging in normal female rats, adipose tissue activity was decreased while cardiac and skeletal muscle activities were increased relative to males of the same age or body weight. Castration of male rats failed to reproduce the effect of estrogens on tissue lipoprotein lipase. These in vitro data suggest that exogenous estrogens may shift the flux of triglyceride fatty acids from storage in the adipose organ toward incorporation by muscle. These, and other data, raise the possibility that physiological estrogen secretion exerts a tonic influence over the synthesis and ultimate destination of triglyceride fatty acids.
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PMID:Estrogen treatment and gonadal function in the regulation of lipoprotein lipase. 97 48

In order to define specific metabolic abnormalities of adipose tissue metabolism in endogenous hypertriglyceridemia (EH) patients with this condition were compared with normolipidemic controls matched for body fat and fat cell size. In vitro the enlarged fat cells of EH were found to have an increased basal and noradrenaline-stimulated lipolysis in comparison with cells of the same size from normolipidemic controls. The insulin inhibition of noradrenaline-stimulated lipolysis was blunted. Lipoprotein lipase activity in these cells was clearly depressed. Basal triglyceride synthesis from labeled glucose was low in relation to plasma insulin. The reduction of insulin tolerance in vivo suggested that the depression of plasma glycerol and free fatty acid concentration was small in EH, suggesting that the more detailed findings in vitro were of relevance for in vivo conditions. It was suggested that the hyperinsulinemia and decreased glucose tolerance of EH may well be responsible for some of the aberrations of adipocyte metabolism in EH. The decreased responsiveness of lipolysis to insulin and the low lipoprotein lipase activity are, however, findings not typical for enlarged fat cells exposed chronically to insulin and might be characteristic for the fat cells of EH. It seems of importance to further define the factor(s) responsible for these metabolic aberrations, because the abnormalities of the acipocyte metabolism in EH may well offer a possible explanation to the pathogenesis of that condition.
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PMID:Adipocyte metabolism in endogenous hypertriglyceridemia. 119 32

We have studied the levels of total triglycerides, total cholesterol and high, low and very low density lipoproteins, in serum from undernourished children and from eutrophic controls matched by age, race and socioeconomical condition with the undernourished group. Malnourished children were classified according to the severity of the nutritional deficiency and according to the presence or absence of associated overt infections. Serum lipids fractions were evaluated by colorimetric procedures and by electrophoretic isolation and elution of the desired lipoprotein followed by colorimetric evaluation of the cholesterol content. Increased levels of total triglycerides and very low density lipoproteins were observed in the undernourished group. The rise in the levels of total triglycerides and very low density lipoproteins was more marked in children with moderate and severe undernutrition as well as in undernourished with associated overt infection. In contrast, as expected, serum levels of total cholesterol, high density and low density lipoproteins were significantly diminished in undernourished children. The depression in the amount of total cholesterol, high density and low density lipoproteins was more marked in the severe forms of undernutrition. Increased levels of total triglycerides and very low density lipoprotein could be determined by a defect in the clearance of these lipid fractions due to depressed activity of lipoprotein lipase.
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PMID:[Changes in the serum lipid fractions of malnourished children with and without clinical infection. Paradoxical hypertriglyceridemia in malnutrition]. 134 58

The low milk fat syndrome most commonly occurs in dairy cows fed diets with a high ratio of carbohydrate to roughage. It is characterized by markedly depressed yields of milk fat. Rumen buffers, such as sodium bicarbonate (NaHCO3) and magnesium oxide (MgO), are known to correct the milk fat depression observed on restricted roughage rations, although by apparently different mechanisms. The mode of action of NaHCO3 can be explained by control of the proportion of ruminal propionate via control of rumen pH. Cows fed diets supplement with NaHCO3 showed increased feed intake and improved digestibility of dry matter or fibre. The mechanism by which Mg increases milk fat concentration may operate at both rumen and tissue level. Most studies with MgO have suggested that it acts as a buffer or neutralizer in either the rumen or the intestine. During digestion, the addition of MgO increases digestibility of dry matter, as does NaHCO3. Among many different tissue effects, MgO supplementation increases triglyceride uptake by the mammary gland. Feeding MgO tends to increase lipoprotein lipase activity in the mammary gland and to decrease the linoleic acid content of milk fat. The percentage uptake of triglycerides from lipoproteins and milk fat by the mammary gland was greater in cows fed MgO-supplemented rations than in cows fed restricted roughage rations. Triglyceride-rich lipoprotein concentrations are uniquely low in cow plasma compared to other species, but still account for a major portion of the arteriovenous difference in plasma lipids across the mammary gland.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Low milk fat syndrome and magnesium oxide supplementation. 179 52

The effects on body fat accumulation of long-term feeding of high fat diets of differing fatty acid composition were studied in rats. The rats were meal-fed isoenergetic diets based on safflower oil or beef tallow for 4 mo. Each diet was freshly prepared every day throughout the experimental period. Oxygen consumption and carbon dioxide production for 6 h after meals were measured between the 50th and 54th d of the experimental period. Oxygen consumption for 3 h after meals was significantly greater in the safflower oil diet group than in the beef tallow diet group, indicating greater diet-induced thermogenesis in the former group. From the assessment of respiratory quotient, the fat oxidation rate was also higher in the former. After the experimental period (4 mo), body fat accumulation was significantly less in the rats fed safflower oil. This difference was, at least in part, ascribed to increased diet-induced thermogenesis and fat oxidation. Serum triacylglycerol level was markedly lower in the rats fed safflower oil than in those fed beef tallow. The lipoprotein lipase activities in heart and soleus muscle after meals appeared to be higher in the former than in the latter. These results suggest that the consumption of the safflower oil diet increased lipoprotein lipase activity in heart and skeletal muscle, resulting in the elevation of fat oxidation rate and the depression of serum triacylglycerol level.
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PMID:Less body fat accumulation in rats fed a safflower oil diet than in rats fed a beef tallow diet. 223 Oct 19

In an attempt to elucidate the mechanisms underlying retinoid-induced hyperlipidemia, the effects of etretinate (Tigason) and isotretinoin (Roaccutane) on two different plasma fat elimination variables and on the plasma fatty acid composition were studied. Twelve patients with various hyperkeratotic disorders participated in a double-blind cross-over study of etretinate and isotretinoin. Each drug was given for 8 weeks with an 8-week intermission. On five occasions an intravenous fat tolerance test (IVFTT) was performed and the lipoprotein lipase activity (LPLA) in adipose tissue and skeletal muscle was measured. Isotretinoin significantly reduced the fat elimination rate as measured by IVFTT (p less than 0.001) and also decreased the muscle LPLA (p less than 0.05). The etretinate-induced depression of these variables was not statistically significant. The LPLA of adipose tissue and the plasma fatty acid composition were not markedly altered by any of the drugs. The observed changes are probably not sufficient to entirely explain retinoid-induced hyperlipidemia but the results strengthen the opinion that plasma lipid metabolism is more unfavourably affected by isotretinoin than etretinate.
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PMID:Plasma fat elimination tissue lipoprotein lipase activity and plasma fatty acid composition during sequential treatment with etretinate and isotretinoin. 243 78

Within 1 hr of intraperitoneal administration of 1 microgram 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)/kg, lipoprotein lipase (LPL) activity was reduced 38% from initial levels in the adipose tissue of the guinea pig. Maximal depression was observed after 2 days and persisted throughout the 10-day observation period. Oral administration of glucose restored LPL activity in TCDD-treated animals after 1 day but only partially after 2 and 5 days, and had no effect after 10 days of exposure. Although initial (2-day) serum insulin levels were depressed, the inability of glucose to restore LPL activity after prolonged exposure was not due to malabsorption of glucose nor to changes in serum thyroxine or insulin concentration. TCDD also inhibited the lipolytic pathway in the adipocyte, but had no effect on hormone sensitive lipase (HSL). Since HSL and LPL are reciprocally regulated, it was concluded that TCDD acts on the adipocyte to uncouple HSL-LPL reciprocity as well as to reduce LPL production.
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PMID:Reduction of adipose tissue lipoprotein lipase activity as a result of in vivo administration of 2,3,7,8-tetrachlorodibenzo-p-dioxin to the guinea pig. 328 12

The role of the macrophage system in shock pathogenesis now embraces both classic endocytic functions as well as the more recently discovered function of the macrophages as a multifaceted secretory apparatus. Among the major macrophage secretory products are the monokines, regulatory proteins that mediate via both local or paracrine and systemic or endocrine mechanisms, the nonspecific host defense and metabolic responses to inflammation and sepsis. Evidence is reviewed for a monokine involvement in the alterations of protein, fat, and carbohydrate metabolism in sepsis and/or endotoxicosis, viz., enhanced muscle proteolysis, enhanced hepatic acute phase protein synthesis, depressed lipogenesis and lipoprotein lipase function, enhanced peripheral glucose oxidation, and depression of hepatic gluconeogenesis. Monokines are also related to the disturbed endocrine mechanisms of sepsis, viz., enhanced insulin secretion and depressed adrenal steroidogenesis. It is suggested that the macrophage system mediates via secretion of monokines an integrated fuel substrate and hormonal adjustment to sepsis, which on the one hand may provide optimal metabolic homeostasis for systemic host defense, but on the other hand, if allowed to act unchecked, may contribute to the metabolic dyshomeostasis of septic shock.
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PMID:Monokines and the metabolic pathophysiology of septic shock. 388 Dec 89


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