Release of Clearing Factor Lipase (Lipoprotein Lipase) in Vivo and from Isolated Perfused Hearts of Alloxan Diabetic Rats

Aktin, E; Meng, H. C.

doi:10.2337/diab.21.3.149

Cited by 23 publications

(14 citation statements)

References 6 publications

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“…In patients with T2DM LpL mRNA, protein expression and activity were significantly decreased in skeletal muscle 35, 36 . Conflicting results have been reported in studies of LpL activity in the heart and the skeletal muscles in STZ-treated rodents: Both decreased 53 and increased 54 activity levels have been observed. The reported differences might relate to the length as well as severity of diabetes and methodological differences, e.g.…”

Section: Discussionmentioning

confidence: 89%

Lipolysis, and Not Hepatic Lipogenesis, Is the Primary Modulator of Triglyceride Levels in Streptozotocin-Induced Diabetic Mice

Willecke

Scerbo

Nagareddy

et al. 2015

ATVB

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Objective Diabetic hypertriglyceridemia is thought to be primarily driven by increased hepatic de novo lipogenesis. However, experiments in animal models indicated that insulin deficiency should decrease hepatic de novo lipogenesis and reduce plasma triglyceride levels. Approach and Results To address the discrepancy between human data and genetically altered mouse models, we investigated whether insulin deficient diabetic mice had triglyceride changes that resemble those in diabetic humans. Streptozotocin (STZ)–induced insulin deficiency increased plasma triglyceride levels in mice. Contrary to the mouse models with impaired hepatic insulin receptor signalling, insulin deficiency did not reduce hepatic triglyceride secretion and de novo lipogenesis-related gene expression. Diabetic mice had a marked decrease in postprandial TG clearance, which was associated with decreased lipoprotein lipase (LpL) and PPARα mRNA levels in peripheral tissues and decreased LpL activity in skeletal muscle, heart and brown adipose tissue. Diabetic heterozygous LpL knockout mice had markedly elevated fasting plasma triglyceride levels and prolonged postprandial TG clearance. Conclusion Insulin deficiency causes hypertriglyceridemia by decreasing peripheral lipolysis and not by an increase in hepatic TG production and secretion.

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Section: Discussionmentioning

confidence: 89%

Lipolysis, and Not Hepatic Lipogenesis, Is the Primary Modulator of Triglyceride Levels in Streptozotocin-Induced Diabetic Mice

Willecke

Scerbo

Nagareddy

et al. 2015

ATVB

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“…14 " 16>38>39 The effect of insulin on myocardial LPL is still under dispute. The nonfunctional enzyme located in extravascular myocardium may be insulin-sensitive, 40 whereas total myocardial LPL has been reported to be insulin-independent. 1439 The activity of LPL in different tissues of insulindeficient human diabetics is not known.…”

Section: Discussionmentioning

confidence: 99%

Postheparin Plasma Lipoprotein Lipase and Hepatic Lipase in Diabetes Mellitus: Relationship to Plasma Triglyceride Metabolism

1977

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The activity of two triglyceride lipases was determined by an immunochemical method in the postheparin plasma of 60 diabetic patients and of 47 age- and sex-matched nondiabetic control subjects. The results were related to the type of diabetes, to plasma triglyceride and insulin concentrations, to removal of exogenous fat from the blood, and to turnover of VLDL-triglycerides . The mean postheparin plasma lipoprotein lipase (LPL) activity was decreased by 44 per cent (p less than 0.001) in patients with untreated ketotic diabetes and by 20 per cent (p less than 0.01) in patients with untreated mild to moderate nonketotic early-onset diabetes. Insulin treatment of ketotic diabetes resulted in a rapid increase in the activity of LPL and decrease in serum triglycerdie level, whereas sulfonylurea treatment of non-insulin-requiring diabetics did not significantly influence the enzyme activity. In insulin-treated chronic diabetics the average postheparin plasma LPL activity was not different from that of nondiabetic controls, but some of these patients had high LPL values. In normolipidemic maturity-onset-type diabetics the LPL activity was within normal range, but in those having hypertriglyceridemia the average LPL value was decreased by an average of 26 per cent (p less than 0.01). The LPL activity showed a significant negative correlation with the logarithm of serum triglyceride concentration (r = -0.62) and a positive correlation with fractional removal of Intralipid (r = +0.64) and fractional turnover of V triglyceride (r = +0.40). The activity of LPL was correlated to basal plasma insulin concen tration in the insulin-deficient diabetes r = +0.34) but not in patients with maturity-onset-type diabetes. The hepatic lipase (HL) activity of postheparin plasma was similar in diabetes and controls, with the exception of hypertriglyceridemic maturity-onset diabetics, who had higher mean HL activity than the corresponding control group (p greater than 0.01). The activity of HL was not related to triglyceride removal but showed a significant correlation to VLDL-triglyceride production rate. On the basis of these results it seems that a deficiency of LPL accounts for a great deal of the elevation of serum triglyceride in insulin-deficient human diabetes but has a smaller role in the pathogenesis of the hypertriglyceridemia that is associated with maturity-onset diabetes. The latter abnormality is caused mainly by an increased secretion of triglycerides into the blood even though a decreased LPL may contribute to development of hyperlipemia in cases with gross elevation of serum triglycerides.

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“…Since the isolation of lipoprotein lipase from the defatted preparation of heart tissues by Korn (1955a,b), there have been numerous reports on the occurrence as well as purification of lipoprotein lipase from rat heart (Aktin & Meng, 1972;Twu et al, 1975), cultured myocardial cells (Henson et al, 1977;Chajek et al, 1977) and isolated adult rat myocytes (Bagby et al, 1977;Chohan & Cryer, 1978). Lipoprotein lipase has been demonstrated to be multiphasic in rat heart (Aktin & Meng, 1972).…”

Section: Discussionmentioning

confidence: 99%

“…Lipoprotein lipase has been demonstrated to be multiphasic in rat heart (Aktin & Meng, 1972). It has been postulated that in the heart the lipoprotein lipase exists in functional and non-functional form and that the functional lipoprotein lipase is formed in sites that are not accessible to heparin and then transported to the site of action (Chajek et al, 1975;Borensztajn et al, 1975 (Robinson, 1963;Robinson & Jennings, 1965;Chohan & Cryer, 1978), (ii) homogenates of fresh tissues (Mallov & Alousi, 1967;Mallov & Cerra, 1967;Chohan & Cryer, 1978) and (iii) 12000g supernatants (Bagby et al, 1977).…”

Section: Discussionmentioning

confidence: 99%

Differences in the metabolism of very-low-density lipoproteins by isolated beating-heart cells and the isolated perfused rat heart. Evidence for collagenase-released extracellular lipoprotein lipase

Rajaram¹,

Clark²,

Barter³

1980

Biochemical Journal

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1. The metabolism of VLD lipoproteins (very-low-density lipoproteins) was studied in intact isolated beating-heart cells and isolated perfused rat heart from starved animals by using ['4C] lipase activity was largely undetectable in the homogenate of the isolated heart cells. 6. It is concluded that the lipoprotein lipase responsible for the hydrolysis of VLD lipoprotein triacylglycerol is predominantly located externally to the heart muscle cells and that its release can be facilitated by perfusion of the heart with bacterial collagenase.

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Release of Clearing Factor Lipase (Lipoprotein Lipase) in Vivo and from Isolated Perfused Hearts of Alloxan Diabetic Rats

Cited by 23 publications

References 6 publications

Lipolysis, and Not Hepatic Lipogenesis, Is the Primary Modulator of Triglyceride Levels in Streptozotocin-Induced Diabetic Mice

Lipolysis, and Not Hepatic Lipogenesis, Is the Primary Modulator of Triglyceride Levels in Streptozotocin-Induced Diabetic Mice

Postheparin Plasma Lipoprotein Lipase and Hepatic Lipase in Diabetes Mellitus: Relationship to Plasma Triglyceride Metabolism

Differences in the metabolism of very-low-density lipoproteins by isolated beating-heart cells and the isolated perfused rat heart. Evidence for collagenase-released extracellular lipoprotein lipase

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