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T S Larsen

Publications and source records attributed to T S Larsen.

48 records · Page 3Linked to original sources
PubMed1987

Triacylglycerol lipase activities in isolated myocardial cells from chronically diabetic rat hearts.

Diabetes was induced by the administration of streptozotocin (55 mg/kg or 70 mg/kg) to rats. After 21-25 days, myocardial cells (myocytes) were isolated from control and diabetic rat hearts. Rates of endogenous lipolysis, measured as the output of glycerol, were elevated in the chronically diabetic myocytes. Lipoprotein lipase activity was reduced in homogenates of diabetic myocytes. Neutral triacylglycerol lipase activity was increased in myocytes from rats made diabetic with the lower dose of streptozotocin, but not in myocytes from diabetic rats given the higher dose. Diabetes had no effect on acid lysosomal lipase activity.

Animals↗
PubMed1987

Methylamine does not inhibit rates of endogenous lipolysis in isolated myocardial cells from rat heart.

Triacylglycerol lipase activity with a pH optimum of 5 was present in homogenates of myocardial cells from rat heart. Acid lipase activity was inhibited by serum, heparin, and increased ionic strength. Methylamine, a lysosomotropic agent, did not inhibit the basal or isoproterenol-stimulated rate of endogenous lipolysis as measured by glycerol output from control myocytes. Similarly, accelerated rates of glycerol output that are a consequence of an elevation in the intracellular stores of triacylglycerols in myocytes from diabetic rat hearts and from myocytes prepared with free fatty acids in the isolation solutions were not reduced by methylamine. Therefore, the acid lysosomal triacylglycerol lipase must not be involved in the mobilization of endogenous triacylglycerols in myocardial cells from rat heart.

Animals↗
PubMed1985

Seasonal changes in lipogenesis and lipolysis in isolated adipocytes from Svalbard and Norwegian reindeer.

Arctic reindeer exhibit marked seasonal changes in fat deposition and mobilization. At intervals throughout the year, therefore, we have measured feed intake of both Svalbard (SR) and Norwegian reindeer (NR) together with the seasonal changes in size, lipogenic and lipolytic capacity of isolated adipocytes from both sub-species. Feed intake of both NR and SR was maximal in August, but declined thereafter, reaching minimum values in January (NR) and March (SR), 55 and 69% below the August value, respectively. NR and SR adipocyte volume changed in parallel and were reduced to the same extent (69%) from their maximum in August to their minimum in May. Adipocyte lipogenic capacity, measured as acetate incorporation into cellular lipid at saturated acetate concentrations, was lowest in January (NR adipocytes) and March (SR adipocytes), 92 and 90%, respectively, below the maximum values, which were obtained in August. Lipolytic capacity, measured as maximum adrenaline-stimulated glycerol release, was high in SR adipocytes from March through to October and in NR adipocytes from July through to January. Minimum lipolytic capacity, on the other hand, was found in January (SR adipocytes) and March (NR adipocytes). The present findings may be explained by alterations in lipogenic enzyme activity and in the lipolytic activation system.

Adipose Tissue↗
PubMed1985

Seasonal changes in blood lipids, adrenaline, noradrenaline, glucose and insulin in Norwegian reindeer.

Plasma concentrations of free fatty acids (FFA), glycerol, adrenaline, noradrenaline, glucose and insulin, as well as serum concentrations of triacylglycerols, total cholesterol and high density lipoprotein (HDL)-bound cholesterol, were measured at intervals during a I-year period in Norwegian reindeer. Free fatty acids and glycerol were high in January-March, low in April-July, and high again in August-September. Glucose was low in November-February and high but variable in March-October. Triacylglycerols, total and HDL-bound cholesterol were all low in November-March, but increasing in April and reaching a peak in August-September. Plasma noradrenaline and adrenaline did not change significantly throughout the year. Plasma insulin was low in October-April, increasing significantly from June-August/September. The seasonal changes in the serum concentrations of triacylglycerols, total and HDL-bound cholesterol, as well as the plasma concentration of glucose, coincided with the seasonal changes in food intake. Free fatty acids and, to some extent, glycerol were, in contrast, inversely related to feed intake. It is suggested that insulin may play an important role in the long-term regulation of fat mobilization, while the importance of catecholamines in this respect is questionable.

Animals↗
PubMed1985

Effects of prolonged food restriction on some aspects of lipid metabolism in Norwegian and Svalbard reindeer.

The high-arctic Svalbard reindeer (SR) deposit great amounts of body fat in autumn for subsequent use during winter when food is often in short supply. Captive SR and, for comparative reasons, the sub-arctic Norwegian reindeer (NR) were offered 15% of their ad libitum food intake during a 21-day period in September/October and its effect on fat metabolism was investigated. Plasma free fatty acids (FFA), glycerol, glucose, insulin and urea as well as lipogenic and lipolytic activity of isolated adipocytes were determined. Levels of FFA and glycerol increased immediately when food intake was restricted, reaching the highest levels in SR. Plasma glucose was fairly constant in NR, but decreased in SR. Plasma insulin decreased in both species. Plasma urea increased steadily from day 5 in NR and from day 11 in SR, after a transient rise on day 1 in both. Lipogenic activity had vanished completely in both NR and SR adipocytes when tested after 13 days of food restriction, while lipolytic activity was initially increased, after which it decreased in adipocytes from both species. After 21 days of food restriction SR adipocytes exhibited another marked increase in lipolytic activity, while the fat deposits of NR at that time were too small to allow examination. Thus, reindeer do not differ from other species in their lipogenic responses, although they show some hitherto undescribed lipolytic responses to prolonged food restriction.

Adipose Tissue↗
PubMed1985

On the hormonal regulation of lipolysis in isolated reindeer adipocytes.

The effects of insulin and bovine growth hormone (bGH) on lipolysis (basal and/or adrenaline-stimulated) were investigated in isolated adipocytes from the Norwegian reindeer. Addition of 100 nmol l-1 adrenaline to the cells increased lipolysis 20-fold above basal lipolytic rate. Insulin (0.I and I nmol l-I) depressed lipolysis significantly at submaximal adrenaline stimulation but had no effect when lipolysis was stimulated maximally. Bovine GH (25 and 100 ng ml-I) inhibited basal lipolysis during the first 2 h of incubation, whereas refractoriness to this action was induced during the third and fourth hour of incubation. These effects were not influenced by inclusion of a small amount of glucocorticoid (dexamethasone, 25 ng ml-I). Addition of 0.I and I nmol l-I insulin together with bGH (100 ng ml-I) prevented the initial antilipolytic effect of the latter and resulted in the expression of normal basal lipolytic rates. Preincubation with bGH (100 ng ml-I) for 2 h did not alter the lipolytic response of the adipocytes to adrenaline. These findings lend support to the conclusion that insulin exerts a major control of lipolysis in reindeer adipose tissue. The significance of the antilipolytic effect of bGH is difficult to evaluate since this effect was transient and was abolished during the third and fourth hour of incubation.

Adipose Tissue↗
PubMed1983

Effects of volatile fatty acids and ketone bodies on lipolysis in isolated adipocytes from Norwegian reindeer (Rangifer tarandus).

The effect of volatile fatty acids (acetate and propionate) and ketone bodies (acetoacetate and DL-3-hydroxybutyrate) on adrenaline stimulated lipolysis have been studied in isolated adipocytes from Norwegian reindeer. All four substances caused a strong (63-90%) inhibition of lipolysis, measured as glycerol release, at low concentrations of adrenaline (5 nM). At higher adrenaline concentrations (50 nM) inhibition only took place in the presence of propionate (30% inhibition) or DL-3-hydroxybutyrate (43% inhibition). DL-3-hydroxybutyrate caused a marked reduction in adrenaline stimulated glycerol release, even at very low concentrations. The effective dose causing 50% inhibition (ED50) was 1.5 mM. It is suggested that both volatile fatty acids and ketone bodies can act as important volatile regulators of lipopolysis in this high arctic ruminant undergoing great seasonal changes in volatile fatty acid and supposedly ketone body production.

3-Hydroxybutyric Acid↗
PubMedDate not supplied

Phospholipase C-evoked glycerol release in energy depleted rat myocardial cells.

Preincubation of rat myocardial cells in hypoxic substrate-free Krebs-Ringer bicarbonate buffer (pH 7.4, 37 degrees C) resulted in a substantial decline in high energy phosphates (ATP and CP). Thus, 20 and 60 min preincubation produced a 18 and 72% decline in ATP content, whereas the parallel decline in CP content was 51 and 73%. This energy depletion was accompanied by a change in cell morphology from the initial rod-shaped form to rounded up (hyper-contracted) myocytes. In cells preincubated in substrate-free normoxic buffer, both normal morphology and energy homeostasis were maintained. When energy depleted myocytes later were incubated in the presence of phospholipase C (PLC), this resulted in a substantial release of glycerol, amounting to 92 and 137 nmol/10(6) cells.2 h in 20 and 60 min energy depleted myocytes, respectively. In addition, PLC caused an increased leakage of lactate dehydrogenase in energy depleted myocytes. Normal cells, on the other hand, were apparently not affected by PLC. These data suggest that PLC selectively attacks energy depleted and/or structurally damaged myocytes. This could well enhance the breakdown of the natural barrier between the extra- and intracellular compartments and thus augment the cellular damage during ischemia. Moreover, energy depleted myocytes appeared exceptionally sensitive to this enzyme, since the levels required to cause glycerol or lactate dehydrogenase release were several orders of magnitude lower than that required to cause membrane permeation in other cell types.

Adenosine Triphosphate↗
PubMedDate not supplied

Effects of hypoxia on lipolysis in isolated rat myocardial cells.

The effect of hypoxia on myocardial lipolysis (glycerol release) was investigated in freshly isolated, calcium-tolerant rat ventricular myocytes. Hypoxia was produced by gassing the incubation medium (Joklik-minimum essential medium, supplemented with 1.2 mM MgSO4, 1 mM DL-carnitine, 1.5 mM CaCl2 and 0.6 mM palmitate bound to 0.15 mM fatty acid free bovine serum albumin) with 95% N2-5% CO2. Control (normoxic) incubations were carried out under air-5% CO2 atmosphere. Basal glycerol release increased from 46.6 +/- 3.0 nmol/10(6) cells.30 min in normoxia to 64.5 +/- 4.3 nmol/10(6) cells.30 min in hypoxia (p less than 0.05). Addition of isoprenaline (10 microM) resulted in a significant (p less than 0.05) stimulation of the glycerol release both in normoxia and in hypoxia, but the enhancement above basal rates was apparently lower in hypoxia (8.7 +/- 2.5 nmol/10(6) cells.30 min) than in normoxia (12.2 +/- 2.7 nmol/10(6) cells.30 min). Furthermore, whereas the isoprenaline-induced rise in lipolysis both in normoxia and hypoxia was prevented by inclusion of propranolol (10 microM), propranolol did not affect the hypoxia-induced increase in lipolysis. Thus, the above findings suggest that myocardial lipolysis may be stimulated by local non-adrenergic mechanisms during hypoxia.

Animals↗
PubMedDate not supplied

Effect of stimulation and veratrine on total cellular calcium in rat and guinea-pig ventricular myocytes.

In rat cardiac myocytes, calcium efflux by Na+/Ca(2+)-exchange is expected only during ventricular systole following initial action potential repolarization. In contrast, in guinea-pigs, calcium influx via Na+/Ca(2+)-exchange is expected only during the initial portion of the action potential. Thus electrical stimulation is expected to result in reduced intracellular calcium ([Ca2+]i) in rat and an increase in guinea pig. We tested this hypothesis by measuring total cellular calcium ([Ca]tot) using 45Ca following stimulation of isolated rat and guinea-pig ventricular myocytes. Many studies have also emphasized that the rate and the direction of Na+/Ca(2+)-exchange across the sarcolemma are in part dependent on the magnitude of the transsarcolemmal sodium gradient. Thus, increasing intracellular sodium ([Na+]i) is expected to result in an increased [Ca2+]i. This hypothesis was also tested by measuring [Ca]tot following veratrine administration. Enzymatically isolated rat and guinea-pig ventricular myocytes were divided into two groups; non-stimulated and stimulated (1 Hz). The concentration-dependent effects of veratrine (1,10,100 micrograms/ml) on [Ca]tot were determined in both these groups. In the absence of veratrine, non-stimulated rat myocytes had a significantly higher [Ca]tot than did stimulated ones. Non-stimulated guinea-pig myocytes had a significantly lower [Ca]tot when compared with stimulated ones. Veratrine increased [Ca]tot in both species in a concentration-dependent fashion. In addition, following veratrine the difference between [Ca]tot in non-stimulated and stimulated rat myocytes was no longer significant. These results support those of others who have demonstrated that stimulation is associated with a gain of cellular calcium in both rabbit and guinea-pig ventricle and a calcium loss in rat ventricle.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Phosphatidylcholine metabolism in hypoxic and phospholipase C exposed rat ventricular myocytes.

A phospholipase C specific for choline and ethanolamine acyl and plasmalogen glycerophospholipids (PC-PLC) has been described in myocardial tissue. In the present study we investigated whether an endogenous PC-PLC is activated in hypoxic, substrate-free incubations of rat ventricular myocytes. The phosphatidylcholine pool of the myocytes was prelabelled with [14C]choline during a 4-h preincubation (pulse) period. The myocytes were subsequently washed and incubated for another 2 h (chase period) in normoxic, hypoxic, or hypoxic buffer supplemented with PC-PLC from Bacillus cereus. We hypothesized that an increase in the total (intracellular plus extracellular) content of [14C]phosphocholine (one of the products resulting from PC-PLC action on phosphatidylcholine) throughout the chase period would indicate PC-PLC activity. Instead, an apparent decrease was observed for this parameter in all myocyte groups (17-29%), even in the one exposed to exogenous PC-PLC. However, 60 min after the start of the chase period, the level of total [14C]phosphocholine was higher in hypoxic (p = 0.022) and hypoxic + PC-PLC exposed (p = 0.013) myocytes compared with normoxic controls. The total content of [14C]choline increased significantly (p < 0.017) in all myocyte groups during the incubation period (98-153%) as a result of an increment of this metabolite in the buffer. Furthermore, the values measured in hypoxic and hypoxic + PC-PLC exposed myocytes during the first hour of the chase period were significantly (p < 0.017) higher than the corresponding values in normoxic myocytes. The present results do not allow firm conclusions regarding endogenous PC-PLC activation in energy-depleted rat cardiac myocytes.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗