Induction of adipose tissue lipoprotein lipase by nicotinic acid

Nikkilä, Esko A.; Pykälistö, Olavi

doi:10.1016/0005-2760(68)90055-6

Cited by 51 publications

(11 citation statements)

References 16 publications

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“…The association of enhanced lipolysis and impaired triglyceride clearance observed in these diabetic patients is not surprising since the enzymes, triglyeeride lipase and lipoprotein lipase, regulating these two processes are known to change in a reciprocal direction in response to a number of physiological and pathological conditions. Thus Shafrir and Biale [~t7] have observed a decrease in adipose tissue lipoprotein lipase during stimulation of lipolysis, and Nikkils and Pyk~list5 [35] found a negative correlation between the rates of mobilisation of fatty acids and the lipoprotein lipase activity in rat adipose tissue. In the present study we have also observed impaired release of lipoprotein lipase into the plasma, in response tO heparin, associated with en-hanced lipolysis.…”

Section: Discussionmentioning

confidence: 99%

“…Elevation in tissue levels of this compound activates triglyceride lipase and inhibits lipoprotein lipase, resulting in enhanced lipolysis and impaired triglyceride clearance. Nikkili~ and Pyk//list5 [35], on the other hand, suggested that the changes in lipoprotein lipase activity in this situation were secondary to the increased intracellular concentration of fatty acids, associated with enhanced lipolysis, which might exert regulatory control over the synthesis of the lipoprotein lipase.…”

Section: Discussionmentioning

confidence: 99%

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Inter-relationship between insulin secretion and plasma free fatty acid and triglyceride transport kinetics in maturity onset diabetes and the effect of phenethylbiguanide (Phenformin)

1974

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Summary. The plasma free fatty acid and triglyceride transport kinetics in 16 non-obese and 7 obese maturity onset diabetics with hypertriglyceridaemia have been compared with results obtained in 27 control subjects. Changes in glucose and insulin responses were evaluated in relation to the lipid parameters. All the diabetics showed elevated plasma FFA levels and turnover rates. In the non-obese diabetics the plasma triglyceride turnover rate was within the normal range and their hypertriglyceridaemia was due to impaired trigleeride clearance. In the obese diabetics the plasma trig]yceride turnover rate was increased and they also had some impairment of triglyceride clearance, so that in them a double mechanism was observed to account for their hypertriglyceridaemia. The insulin levels in the diabetics were similar to, or greater than, those found in the controls. Our results suggested that the enhanced lipolysis and impaired triglyceride clearance observed in the diabetic patients were a manifestation of insulin unresponsiveness in adipose tissue and that the changes in insulin and glucose relationship could be secondary to elevated FFA and triglyceride levels. Further confirmation was obtained by the finding of an exaggerated insulin response to a glucose challenge in normal subjects infused with Intralipid.Treatment with phenethylbiguanide (Phenformin) significantly lowered the plasma FFA and triglyceride concentration in both diabetic groups. This was associated with normalisation of both plasma FFA turnover and triglyceride clearance. It also reduced the triglyceride turnover rate to the normal range in the obese diabetics. These changes were associated with a fall of plasma glucose and insulin levels to within the normal range. These results suggested an effect of Phenformin in reducing the rate of lipolysis leading to improved glucose tolerance.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Inter-relationship between insulin secretion and plasma free fatty acid and triglyceride transport kinetics in maturity onset diabetes and the effect of phenethylbiguanide (Phenformin)

1974

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“…33 It has also been demonstrated that nicotinic acid, like insulin, depresses adenosine 3',5' monophosphate (cyclic AMP) production in the rat epididymal fat pad. 34 Similar insulin-like effects of nicotinic acid on liver might substantially explain its protective effect on glucokinase, since insulin added in vitro has been shown to protect glucokinase activity in the perfused rat liver.…”

Section: Discussionmentioning

confidence: 99%

Effect of Acute Insulin Deprivation on Rat Liver Glucokinase

Ruderman

Lauris

1968

Diabetes

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The effect of acute insulin deprivation on hepatic glucokinase was studied in the intact rat. Liver glucokinase decreased by 30 per cent within 3 hrs. after the intravenous -administration of anti-insulin serum (AIS) to fed rats. Hexokinase activity did not change significantly whereas glucose-6-phosphatase activity rose. The administration of glucagon or puromycin failed to decrease glucokinase activity within 3 hrs. despite the fact that the latter agent depressed leucine incorporation into liver protein by 80 per cent. Subcutaneous administration of nicotinic acid significantly reduced the AIS induced fall in glucokinase. In •addition, it completely prevented the rise in serum free fatty acids and also diminished the rise in blood glucose. These findings suggest that in acute insulin deprivation the immediate fall in glucokinase activity results from an accelerated rate of enzyme inactivation rather than an inhibition of enzyme synthesis. DIABETES i7: 611-16, October, 1968.

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“…More than 50 years ago, Carlson and Oro [42] demonstrated that nicotinic acid led to a 'metabolic type of sympathicolysis' with a rapid decrease in FFA. This was soon confirmed [43] and we have shown that arrhythmias and ST segment elevation or depression occurring during myocardial ischaemia can be reduced by a nicotinic acid analogue [44,45]. Nicotinic acid also depresses FFA extraction across the ischaemic myocardium during basal and isoprenaline stimulated lipolysis [46].…”

Section: Antilipolytic Therapymentioning

confidence: 62%

Fatty acids and the risk of death during acute myocardial ischaemia

Oliver

2014

Clinical Science

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Plasma free fatty acids (non-esterified fatty acids) increase in the first hour of the onset of acute myocardial ischaemia. This results from catecholamine stimulation of adipose tissue lipolysis. It can lead to a metabolic crisis in the injured myocardium with the development of ventricular arrhythmias and increased early mortality. Preconditioning, β-adrenergic blockade and glucose-insulin-potassium are possible therapeutic approaches, but anti-lipolytic agents, such as some nicotinic acid derivatives, can reduce plasma free fatty acid concentrations within minutes and have untried potential. A clinical trial of their effectiveness is needed from the first moment when a patient with an acute coronary syndrome is seen by paramedics.

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Induction of adipose tissue lipoprotein lipase by nicotinic acid

Cited by 51 publications

References 16 publications

Inter-relationship between insulin secretion and plasma free fatty acid and triglyceride transport kinetics in maturity onset diabetes and the effect of phenethylbiguanide (Phenformin)

Inter-relationship between insulin secretion and plasma free fatty acid and triglyceride transport kinetics in maturity onset diabetes and the effect of phenethylbiguanide (Phenformin)

Effect of Acute Insulin Deprivation on Rat Liver Glucokinase

Fatty acids and the risk of death during acute myocardial ischaemia

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