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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Functional lipoprotein lipase activity was recently described in rat brain. The present study was performed to further characterize the biologic significance of brain lipoprotein lipase (heparin releasable component) and elucidate regulatory factors. Comparative studies were performed on tissue (brain, adipose, and heart) heparin releasable lipoprotein lipase in the fasted and diabetic (streptozotocin 100 mg/kg BW IP) rat. Both fasting (96 hours) and diabetes (ten days) significantly decreased brain (cortical) (P less than .05) and adipose (epididymal fat pad) (P less than .001) lipoprotein lipase activity. In contrast, heart muscle enzyme activity was significantly increased (P less than .001) in response to fasting and diabetes. Refeeding (Purina chow 96 hours) and insulin replacement (96 hours) reversed these changes in tissue lipoprotein lipase consequent to fasting and diabetes, respectively. There was a positive correlation between the changes in serum insulin concentration and adipose lipoprotein lipase, but there was no correlation between this parameter and brain or heart lipoprotein lipase. In addition, although T3 therapy normalized the low T3 state associated with both fasting and diabetes, it had no effect on the enzyme activity in the studied tissues. However, subsequent studies demonstrated that hypothyroidism (2 weeks post thyroidectomy) significantly decreased brain lipoprotein lipase activity (P less than .001) and increased both the adipose (P less than .025) and heart (P less than .025) enzyme activity. T3 replacement (0.8 micrograms/100 BW/d for 1 week) reversed the effects of hypothyroidism. However, the relationship between brain enzyme activity and serum T3 was nonlinear as hyperthyroidism tended to reduce brain LPL activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Brain lipoprotein lipase is responsive to nutritional and hormonal modulation. 330 44

Lipolytic activity was measured in human plasma without prior administration of intravenous heparin. Eluted from heparin-Sepharose in a barbital buffer containing 6 mg/ml heparin, plasma lipolytic activities in 20 subjects were distributed between hepatic triglyceride lipase (HTGL, mean +/- SE 60.6 +/- 4.6%) and extrahepatic lipoprotein lipase (LPL, 39.4 +/- 4.6%). Confirmation of the identities of HTGL and LPL was provided by inhibitory antisera. Preheparin LPL activity was absent in plasma from a patient with type I hyperlipoproteinemia. Both preheparin HTGL and LPL activities correlated with the respective activities measured in plasma obtained 15 min after intravenous injection of heparin (rs = + .774 and + .685, respectively; n = 12). Evidence for the metabolic regulation of preheparin lipases was provided by measurement of significant increases in LPL and HTGL activities after oral glucose ingestion. Overall, preheparin plasma HTGL and LPL activities may reflect ongoing lipoprotein lipolytic activity in tissue beds, and because these measurements do not require the administration of intravenous heparin, they should prove useful for additional studies of short-term regulation of the lipases.
Diabetes 1988 May
PMID:Plasma lipolytic activity. Relationship to postheparin lipolytic activity and evidence for metabolic regulation. 336 Feb 17

In order to determine the metabolic consequences of lipoprotein glucosylation, the glucosylated 125I-VLDL turnover was analyzed in comparison to the native one. Autologous in vitro glucosylated VLDL, separated by affinity chromatography, was injected into a nondiabetic rabbit and the amount of the radioactivity distributed in all lipoprotein fractions measured. Glucosylated--125I-VLDL metabolism versus control--125I-VLDL after six hours were: glc-VLDL = 35 +/- 4.5%, control- VLDL = 35 +/- 4.9%, glc-IDL = 51 +/- 3.8% control-IDL = 31 +/- 4.3% p less than 0.01; glc-LDL = 9 +/- 2.2%, control-LDL = 12 +/- 2.6%; glc-HDL = 5 +/- 1.4%, control-HDL = 22 +/- 2.9% p less than 0.001. A retained turnover of glc-VLDL and prolonged retaining of the triglyceride-rich lipoproteins (VLDL, IDL) in the circulation were found. The results suggest that the incorporation of glucose into lipoproteins may influence the steric configuration of molecules by blocking the sites of the lipolytic action of lipoprotein lipase. The data presented provide strong support for the idea that there are factors other than reduced LPL activity which contribute to defective VLDL removal in diabetes mellitus.
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PMID:Nonenzymatic glucosylation of very-low density lipoprotein alters its metabolism in the rabbit. 344 10

Lipoprotein lipase has a central role in the metabolism of both triglyceride-rich particles and high density lipoproteins, and it is one determinant of both serum triglyceride and HDL concentrations. In man the enzyme activity in both adipose tissue and skeletal muscle is insulin dependent, and therefore it varies in diabetes according to ambient insulin level and insulin sensitivity. In insulin deficiency (untreated Type 1 diabetes) the enzyme activity in both adipose tissue and muscle tissue is low but increases upon insulin therapy. In chronically insulin-treated patients with good control, the enzyme activity in postheparin plasma is increased. In untreated Type 2 diabetic patients, the average enzyme activity in adipose tissue and postheparin plasma is normal or subnormal. Therapy with oral agents or insulin, resulting in good glycemic control, is followed by an increase of LPL activity in both adipose tissue and postheparin plasma. In both Types 1 and 2 diabetes, changes of LPL activity are associated with relevant alterations in lipoprotein pattern. In insulin deficiency with low LPL, serum total and VLDL triglyceride levels are elevated, and HDL concentration is reduced. In chronically insulin-treated patients with high LPL activity, VLDL triglyceride concentrations are normal or subnormal, and HDL level is increased. In untreated Type 2 diabetic patients subnormal LPL activity may contribute to the elevation of serum triglycerides and to the reduction of HDL level.
Diabetes Metab Rev 1987 Apr
PMID:Lipoprotein lipase in diabetes. 355 32

Ethyl 2[5(4-chlorophenyl)pentyl]oxirane-2-carboxylate (POCA) is strongly hypoglycaemic in fasted normal and diabetic rats [H. P. O. Wolf, K. Eistetter and G. Ludwig, Diabetologia 22, 456 (1982)]. POCA was fed for 12 weeks to rats on a standard low-fat (3%) diet at levels of 0.05% and 0.2% to give daily intakes of about 50 and 200 mg/per kg body-wt respectively. This is much more than effective hypoglycaemic doses in fasted rats (5-10 mg/kg body-wt). The animals appeared healthy but they had slightly decreased rates of weight gain compared with the controls. POCA caused a 15% increase in the weight of the myocardium and accumulation of lipid in the liver. Chronic administration of POCA did not cause any large changes in water-soluble blood metabolite concentrations, although VLDL-triacylglycerol and both VLDL and HDL cholesterol concentrations were lowered. There were only small changes in some metabolites of the glycolytic and gluconeogenic pathways and the citrate cycle in liver and skeletal muscle. ATP concentrations were maintained in all groups. There were 2- to 3-fold increases in the total content of CoA and of carnitine and their acylated forms. POCA-feeding caused small decreases in LPL activities in heart and had variable effects in adipose tissue. POCA was also fed to a few rats on a high fat (30%) diet for 4 weeks. Only small changes in blood, liver and muscle metabolite concentrations were found, except for large increases in the liver CoA and carnitine contents. It was concluded that POCA does not cause large perturbations of glucose homeostasis, or acute toxic effects, during 12 weeks administration to normal animals at high dose levels. The very-long term importance of accumulation of lipid in liver; increase in myocardial weight; and also of hepatic peroxisomal proliferation [A. J. Bone, H. S. A. Sherratt, D. M. Turnbull and H. Osmundsen, Biochem. biophys. Res. Commun. 104, 708 (1982)] cannot yet be determined. The possible use of POCA and related compounds in the chemotherapy of diabetes merits further investigation.
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PMID:Metabolic changes in fed rats caused by chronic administration of ethyl 2[5(4-chlorophenyl)pentyl]oxirane-2-carboxylate, a new hypoglycaemic compound. 623 Oct 30

The response of blood glucose and serum lipids and lipoproteins to a high-carbohydrate, high-fiber, low-fat diet was assessed in 10 insulin-dependent diabetic subjects. The diet contained approximately 60% of calories as carbohydrate (CHO) and 20% as fat. The patients were followed for 2 wk in a metabolic ward and subsequently for 4 wk at home without changing insulin dosage. During this 6-wk period, the fasting blood glucose fell from 10.6 +/- 1.1 to 8.9 +/- 1.3 mmol/L (NS); HbA1 fell from 11.7 +/- 0.5 to 11.0 +/- 0.7% (P less than 0.05). Serum total triglyceride and very-low-density lipoprotein levels remained unchanged. After 2 wk in the ward on a high-CHO diet, total cholesterol fell by 15% (P less than 0.01), LDL cholesterol by 16% (P less than 0.001), and HDL cholesterol by 10% (P less than 0.05). The fall of HDL cholesterol was due to a decrease of HDL3 cholesterol only. After the 4-wk home period on a high-CHO diet, the observed lipoprotein changes were reversed. Heparin-releasable adipose tissue LPL activity was not influenced by a high-CHO diet. In conclusion, a high-carbohydrate, high-fiber, low-fat diet did not deteriorate the diabetic control, and it had no unfavorable effects on serum lipids or lipoproteins.
Diabetes Care
PMID:Serum lipids and lipoproteins in insulin-dependent diabetic subjects during high-carbohydrate, high-fiber diet. 630 13

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

These studies were initiated to see if factors other than reduced lipoprotein lipase activity might contribute to the defect in plasma removal of very low density lipoprotein (VLDL) that is observed in insulin-deficient rats. VLDL-triglyceride (TG) was labeled in vivo with 3H-glycerol in control and diabetic rats, and aliquots of plasma containing 3H-VLDL were injected into normal recipient rats. The half-time (t 1/2) of removal was almost twice as long when plasma from diabetic rats was injected, and this was true when the diabetic rats were fed either sucrose or regular chow. A comparable increase in t 1/2 was observed when 3H-VLDL isolated from normal rats was recombined with VLDL-free plasma from control and diabetic rats and injected into normal recipients. As before, the changes observed were not dependent upon antecedent diet. However, no significant difference in t 1/2 was observed when 3H-VLDL was isolated from control and diabetic rats and injected into normal recipients. Thus, there appears to be a factor present in VLDL-free plasma obtained from diabetic rats that interferes with removal of VLDL from the vascular compartment. Whether this factor is found in diabetic plasma in vivo, or is transferred from diabetic VLDL to diabetic plasma in the isolation procedure, remains to be clarified. In either event, there appears to be a factor, other than reduced LPL activity, that may play a role in the defect of VLDL-TG removal seen in insulin deficiency.
Diabetes 1981 Jun
PMID:Evidence for a new cause of defective plasma removal of very low density lipoproteins in insulin-deficient rats. 701 12

Insulin may be important in regulating adipose tissue lipoprotein lipase in the rat. Insulin appears to be necessary for the maintenance of enzyme activity in adipose tissue in humans since it is decreased in untreated diabetes and returns to normal with anti-hyperglycemic therapy. Other than this permissive role of insulin in maintenance of adipose tissue LPL activity in humans, there is little evidence that insulin, by itself, plays a primary role in the regulation of adipose-tissue lipoprotein lipase in man.
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PMID:Insulin and adipose tissue lipoprotein lipase activity in humans. 703 52

Serum lipids were analyzed in 16 patients with active acromegaly. Of these 62.5% had hyperlipidaemia defined as exceeding and 90% fiducial limits of normal controls. The mean serum cholesterol (5.50 mmol/l) and triglyceride (4.09 mmol/l) levels of the patients were significantly higher than those of age-matched normal controls. Type V hyperlipoproteinaemia was observed in two cases and type III hyperlipoproteinaemia in one. There was no difference in the incidence of diabetes between the normolipidaemic (n = 6) and hyperlipidaemic (n = 10) groups. Serum levels of growth hormone in hypercholestelaemic patients (n = 3) were significantly higher than those of normolipidaemic patients and combined hyperlipidaemic patients (n = 5 tended to have higher levels of growth hormone than normolipidaemic patients. In cases developing type III or type V hyperlipoproteinaemia, the activity of hepatic triglyceride lipase of lipoprotien lipase was decreased, but in increased when serum GH levels fell after therapy for acromegaly. It is suggested that 1) growth hormone may play some role on the pathogenesis of hyperlipidaemia associated with acromegaly, and 2) growth hormone has an inhibitory effect on H-TGL and LPL, and so hyperlipoproteinaemia in some cases of acromegaly might be caused by low H-TGL or LPL activity resulting from high growth hormone levels.
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PMID:The incidence and pathogenesis of hyperlipidaemia in 16 consecutive acromegalic patients. 711 4


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