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Biomedical subjects

M R Taskinen

Publications and source records attributed to M R Taskinen.

At least 253 records · Page 14Linked to original sources
PubMed1978

Relation of plasma high-density lipoprotein cholesterol to lipoprotein-lipase activity in adipose tissue and skeletal muscle of man.

Lipoprotein-lipase activity (LPL) was measured in biopsies of adipose tissue and skeletal muscle of normal human subjects, and the results were related to concentrations of cholesterol and triglycerides in plasma lipoproteins. Adipose-tissue LPL activity was significantly higher in females than in males, whereas no sex difference was observed in skeletal-muscle LPL activity. A highly significant positive correlation was present between the plasma high density lipoprotein (HDL) cholesterol level and LPL activity in adipose tissue (r = +0.66, P less than 0.001) but not between HDL and skeletal-muscle LPL. The results suggest that the activity of LPL in adipose tissue and the rate of catabolism of triglyceride-rich lipoproteins might be one of the factors that determine the concentration of HDL in plasma and at least partly account for the known sex difference in plasma HDL level.

Adipose Tissue↗
PubMed1978

Lipoprotein lipase activity in adipose tissue and skeletal muscle of runners: relation to serum lipoproteins.

Physically well-trained people generally have lower VLDL-triglyceride and higher HDL-cholesterol levels than sedentary subjects. To examine the underlying mechanisms of this lipoprotein pattern, we measured the lipoprotein lipase (LPL) activity in needle biopsy specimens of adipose tissue and skeletal muscle of competitive runners and of body weight-matched, physically less-active controls. The active sportsmen were either sprinters, whose training program consisted mainly of athletics of short duration or long distance runners undergoing a strenuous endurance exercise program. In sprinters (all males) the serum lipid and lipoprotein concentrations did not differ significantly from those of controls and the mean LPL activities in muscle and adipose tissue were also similar in these two groups. The long distance runners (both sexes), on the other hand, had higher means levels of HDL-cholesterol than the respective controls. The LPL-activity of both adipose tissue (p less than 0.05) and skeletal muscle (p less than 0.01) was significantly higher in male long distance runners than in control males. Female runners had higher muscle LPL activity than controls (p less than 0.01) but in adipose tissue the difference in LPL activity was not significant. Rough estimates calculated for LPL activity present in whole body adipose tissue and skeletal muscle indicated that total LPL activity was 2.3 times higher in male long distance runners and 1.5 times higher in female long distance runners than in the respective controls. In combined groups of male runners and controls, there was a highly significant positive correlation between the serum HDL-cholesterol level and the LPL activity of adipose tissue expressed per tissue weight (r = +0.72, p less than 0.001) or per whole body fat (r = +0.62, p less than 0.001). The group means of HDL-cholesterol and adipose tissue LPL activity in the five cohorts studied (male sprinters, distance runners and controls and female distance runners and controls) were also positively correlated (r = +0.94). It is concluded that endurance training is associated with an adaptive increase of LPL activity not only in skeletal muscle but also in adipose tissue. These changes are not observed in sprinters who are trained by exercises of shorter duration. The high HDL-cholesterol levels of physically well-trained people are probably accounted for, at least partly, by the increased LPL activity and the concomitant rapid turnover or triglyceride-rich lipoproteins.

Adipose Tissue↗
PubMed1978

Lack of behavioural effects following intraventricular infusion of somatostatin in the conscious goat.

The effect of IV or intracerebroventricular (ICV) administration of somatostatin was studied on the behaviour of conscious goats. The doses of somatostatin infused IV were 100 and 300 microgram for 30 min and 600 microgram for 6 min. The doses infused ICV were 10 and 100 microgram for 30 min and 600 microgram for 6 min. In contrast to earlier reports on experiments with rats ,no behavioral effects whatsoever were seen in goat. IV infusion of 100 to 600 microgram and ICV infusion of 600 microgram of somatostatin caused a difinite reduction in the secretion of insulin and growth hormone, but had no effect on the concentration of blood glucose. The reason why neither IV nor ICV administration of somatostatin had any behavioural effects in the conscious goat, in contrast to the effects in rat, cannot be explained with certainty. This may be due to species specificity, to the amount of somatostatin reaching the central nervous system, or to some metabolic changes in rat but not in goat.

Animals↗
PubMed1978

Effect of acute ethanol load on postheparin plasma lipoprotein lipase and hepatic lipase activities and intravenous fat tolerance.

This study aimed to examine the possibility that ethanol-induced rise of serum triglyceride concentration in man is partly due to an impaired removal of triglycerides from the circulation. Acute ethanol loads given to normal human subjects after an overnight fast reduced the postheparin plasma lipoprotein lipase activity by an average of 25% but did not influence the postheparin plasma hepatic lipase activity or fractional removal of Intralipid triglyceride. When alcolhol was administered to fed subjects in the evening the postheparin plasma hepatic lipase was significantly decreased in the next morning as compared to corresponding control value but the lipoprotein lipase and Intralipid clearance were not changed. It is concluded that the slight decrease of lipoprotein lipase during alcohol intoxication may contribute to the hyperlipemic effect of ethanol.

Ethanol↗
PubMed1977

Response of plasma insulin to small doses of tolbutamide in obesity and acromegaly.

The early response of plasma insulin (IRI) to successive intravenous doses of 50, 100 and 200 mg of tolbutamide was studied in nondiabetic obese subjects, in acromegalic patients, and in healthy controls. The smallest dose raised the plasma IRI level within two minutes in all subjects. The insulin response was correlated with the basal IRI in controls and in obese subjects but not in acromegalic patients. At each tolbutamide dose level the mean IRI response of obese subjects was about three times greater than in controls. In acromegalic subjects an increased response was observed only after the 200 mg dose of tolbutamide. The results suggest that in obesity the stimulus-secretion coupling of insulin output is normal but the number of secretory units is increased. In acromegaly the insulin release pattern is compatible with an increased number of secretory units which, however, are relatively insensitive to tolbutamide, probably due to an elevated serum growth hormone level.

Acromegaly↗
PubMed1975

Ethanol-induced alterations of glucose tolerance, postglucose hypoglycemia, and insulin secretion in normal, obese, and diabetic subjects.

Ethanol at an average blood concentration of 1 mg. per milliliter enhanced the immediate (first-phase) and prolonged (second-phase) insulin response to an intravenous glucose load in nonfasting normal human subjects. Simultaneously, the glucose disposal rate was increased and the postglucose hypoglycemia was accentuated, resulting in definite hypoglycemic symptoms in some individuals. Oral glucose tolerance was not changed by ethanol administration, but the thirty-minute blood glucose and plasma insulin values were increased, suggesting that alcohol might accelerate the absorption of glucose from the gut. Ethanol given orally during evening hours (1.5 gm. per kilogram) caused a nocturnal hyperinsulinemia and a decrease of blood glucose, but not an actual hypoglycemia. Oral glucose tolerance and plasma insulin response tested the next morning, when ethanol had disappeared from the blood, were not influenced by drinking the previous evening. The K-value of intravenous glucose was increased at this time, however. When alcohol was administered for one week at a dose corresponding to 25 per cent of daily calories and substituting for fat, both the oral and intravenous glucose tolerances were impaired in each subject but the insulin response remained unchaged. In obese nondiabetic subjects, ethanol did not potentiate the early insulin response to intravenous glucose but it increased the second phase of insulin secretion in response to sustained hyperglycemia. In contrast to conditions in nonobese subjects, the glucose disposal rate was not incresed and postglucose hypoglycemia was not accentuated by ethanol in overweight subjects. In insulin-deficient diabetic patients the absent early insulin response could not be restored by ethanol, and the late component of insulin release was little increased by alcohol infusion. Ethanol did not improve the glucose utilization of diabetic patients.

Adult↗
PubMed1974

[Hypoglycemia].

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Adenoma, Islet Cell↗