Search PubMed⌕ Search

Biomedical subjects

V A Koivisto

Publications and source records attributed to V A Koivisto.

At least 145 records · Page 8Linked to original sources
PubMed1982

Physical training in juvenile diabetes.

In normal man, physical training increase insulin binding to receptors and body sensitivity to insulin in vivo. In addition, serum lipid and lipoprotein profile changes which may decrease the risk for coronary heart disease. In juvenile onset diabetics, insulin requirements fall during physical training, the mechanism of this decline being yet unknown. There are no prospective studies regarding the prognostic effects of physical training in juvenile diabetes. However, if physical training can improve metabolic control and enhance body sensitivity to insulin resulting in lowered levels of plasma insulin, this may reduce the risk for both micro- and macrovascular complications. The possible adverse effects of exercise, hypoglycemia and excessive rise in counterregulatory hormones can be largely avoided by adequate insulin therapy.

Adult↗
PubMed1981

A rise in ambient temperature augments insulin absorption in diabetic patients.

The absorption rate of 125I-Actrapid insulin (6 U) from a subcutaneous injection site was examined in six insulin-dependent diabetic patients at ambient temperatures of 20 degrees C and 35 degrees C. During a 4-hr observation period, the insulin disappearance rate at 35 degrees C was 50%-60% greater than at 20 degrees C (p less than 0.01). Despite the small dose of insulin used, plasma glucose levels tended to be 1 to 2 mmole/liter lower at 35 degrees C than at 20 degrees C. These findings indicate that a rise in ambient temperature augments insulin absorption, in insulin-treated diabetic patients.

Absorption↗
PubMed1981

Carbohydrate ingestion before exercise: comparison of glucose, fructose, and sweet placebo.

To examine the effect of various carbohydrates on the metabolic and hormonal response to exercise, 75 g glucose, fructose, or placebo were given to nine well-trained males (VO2 max 60 +/- 1 ml . kg-1 . min-1) 45 min before cycle ergometer exercise performed at 75% VO2 max for 30 min. After glucose ingestion, the rise in plasma glucose was 3-fold (P less than 0.005) in plasma insulin 2.5-fold (P less than 0.01) greater than after fructose. During exercise, after glucose administration plasma glucose fell from 5.3 +/- 0.3 to 2.5 +/- 0.2 mmol/l (P less than 0.001) and after fructose from 4.5 +/- 0.1 to 3.9 +/- 0.3 mmol/l (P less than 0.05). The fall in plasma glucose was closely related to the preexercise levels of plasma insulin (r = 0.82, P less than 0.001) and glucose (r = 0.81, P less than 0.001). Both glucose and fructose ingestion decreased the FFA levels by 40-50% (P less than 0.005) and during exercise they remained 30-40% lower after carbohydrate than placebo administration (P less than 0.02). This study suggests that glucose ingestion prior to exercise results in hypoglycemia during vigorous exercise, this rapid fall in plasma glucose is mediated, at least in part, by hyperinsulinemia, and fructose ingestion is associated with a modest rise in plasma insulin and does not result in hypoglycemia during exercise.

Administration, Oral↗
PubMed1980

Sauna-induced acceleration in insulin absorption from subcutaneous injection site.

The effect of the Finnish sauna on insulin absorption from a subcutaneous injection site was examined in eight insulin-dependent diabetic patients by measuring externally the disappearance rate of 125I-labelled rapid-acting insulin. The sauna (twice for 25 minutes at 85 degrees C) accelerated insulin absorption by 110% as compared with room temperature (p < 0.01). After the sauna blood glucose concentrations were 3.0-3.3 mmol/1 (54.1-59.5 mg/100 ml) lower than on the control day (p < 0.05). The fall in blood glucose values was proportional to the increased rate of insulin absorption (r = 0.30; p < 0.01). The hypoglycaemic effect of a sauna in insulin-treated diabetics is clearly at least partly due to enhanced insulin absorption from the injection site. Such an effect might be prevented by taking a snack or reducing the insulin dose.

Absorption↗
PubMed1980

Effects of acute exercise on insulin binding to monocytes in obesity.

The effect of 3 hr of cycle erogmeter exercise on 125I-insulin binding to monocytes was studied in obese and 10 nonobese control subjects. In the basal state before exercise, total specific 125I-insulin binding to monocytes in obese subjects (4.8% +/- 0.3%) was 25% lower than in control subjects (6.6% +/- 0.4%, p less than 0.01). During exercise, insulin binding increased in both groups (p less than 0.05), but the rise in obese subjects was minimal (13% +/- 1%) and was 60%--70% lower than in controls (36% +/- 3%, p less than 0.01). The data indicate that the increment in insulin binding to monocytes induced by acute exercise is diminished in obesity.

Adult↗
PubMed1980

Effects of acute exercise and training on insulin binding to monocytes and insulin sensitivity in vivo.

Insulin binding to monocytes was studied in well-trained long distance runners and in sedentary control subjects in the resting state and after 3 h cycle ergometer exercise at 40% of maximal aerobic power. In addition, in previously untrained subjects we examined the effect of 6 weeks of training on insulin binding to monocytes and insulin sensitivity in vivo. In the athletes at rest, insulin binding to monocytes was 69% higher than in controls (p less than 0.01), and correlated with maximal aerobic power (r = 9.63, p less than 0.05). The rise in insulin binding in the athletes was due to an increase in binding capacity rather than a change in binding affinity. During exercise, insulin binding fell in athletes by 31% (p less than 0.025) in contrast to a 35% rise observed in control subjects (p less than 0.01). As compared to controls, the athletes had a lower respiratory exchange ratio and a smaller decline in plasma glucose during exercise. In previously untrained subjects, physical training resulted in a 35% rise in insulin binding to monocytes (p less than 0.02). The rise in binding was due mainly to an increase in binding capacity. Insulin mediated glucose uptake (as measured by insulin clamp technique) also rose by 30% after physical training (p less than 0.01). The rise in insulin sensitivity was proportional to the improvement in physical fitness (r = 0.81, p less than 0.05). These findings indicate that (a) elevated insulin binding may contribute to the enhanced insulin sensitivity observed after physical training, (b) a fall in insulin binding in athletes during acute exercise may contribute to a greater shift from carbohydrate to fat utilization during exercise in athletes as compared to sedentary controls. These data suggest that physical training may provide a means of reversing or ameliorating abnormalities in insulin binding and sensitivity in insulin resistant states, such as obesity or maturity onset diabetes.

Adult↗
PubMed1980

Alterations in insulin absorption and in blood glucose control associated with varying insulin injection sites in diabetic patients.

In seven insulin-dependent diabetic subjects the disappearance rate of 125I-labelled short-acting insulin from injection sites in the abdominal wall was 86% greater than from the leg (P less than 0.005) and 30% greater than from the arm (P less than 0.05). Absorption from the arm was 40% greater than from the leg (P less than 0.05). The postprandial rise in plasma glucose concentration varied inversely with the rate of insulin absorption and was 30 to 50 mg/dL less after abdominal than after leg injection; the glycemic response after arm injection was intermediate between that after leg and abdominal injection. These results indicate that changing the insulin injection site from the leg to the abdomen or arm accelerates the absorption of insulin and diminishes the postprandial rise in plasma glucose. Varying insulin injection sites within the same anatomic region rather than between different regions may diminish daily variations in insulin absorption and in metabolic control in insulin-dependent diabetic subjects.

Abdominal Muscles↗
PubMed1979

Increased insulin sensitivity and insulin binding to monocytes after physical training.

We studied the effect of physical training on in vivo tissue sensitivity to insulin and insulin binding to monocytes in six previously untrained healthy adults. Physical training (one hour of cycle-ergometer exercise four times per week for six weeks) failed to alter body weight but resulted in a 20 per cent increase (P less than 0.02) in maximal aerobic power (VO2 max) and a 30 per cent increase (P less than 0.01) in insulin-mediated glucose uptake (determined by the insulin clamp technique). The increase in insulin sensitivity correlated directly with the rise in VO2 max (P less than 0.05). Binding of [125I]insulin to monocytes also rose by 35 per cent after physical training (P less than 0.02), primarily because of an increase in the concentration of insulin receptors. Our data indicate that physical training increases tissue sensitivity to insulin in proportion to the improvement in physical fitness. Physical training may have a role in the management of insulin-resistant states, such as obesity and maturity-onset diabetes, that is independent of its effects on body weight.

Adult↗
PubMed1979

The influence of insulin on the lipids in the pulmonary artery and the lungs of severely diabetic rats. A histochemical and chemical study.

The effect of insulin on the triglyceride deposits found in the pulmonary artery branches of streptozotocin-diabetic rats was investigated by treating the animals for two, five, nine or 14 days with insulin (3--8 units/day). Histochemical analysis showed that the triglyceride deposits in the pulmonary artery developed within three to four days after the induction of diabetes, but were not present in any animals five days from the initiation of insulin therapy. Plasma triglycerides, non-esterified fatty acids, phospholipid and total cholesterol concentrations were within the normal range within two days of the inception of insulin therapy and random plasma glucose levels were normal within five days. Analysis of lung lipids showed that after 14 days of insulin treatment the decreased content of phospholipids and the increased content of non-esterified fatty acids found in diabetic rats were also normalized. These findings suggest that insulin has an important role in the regulation of lipid metabolism in the pulmonary artery and lung tissue in the diabetic state.

Animals↗
PubMed1979

Exercise in diabetes: therapeutic implications.

The metabolic response to acute exercise in diabetics is largely determined by the availability of insulin. In nonketotic, insulin-dependent diabetics, acute exercise lowers the level of plasma glucose, whereas in insulin-deficient, ketotic patients, blood glucose may increase during exercise. Exercise accelerates insulin absorption from the exercising limb. Thus, by injecting insulin into a nonexercising area (eg, into the abdomen before leg exercise), the degree of exercise-induced hypoglycemia can be reduced in diabetic patients. Also, elevation in the level of antiinsulin hormones caused by exercise is exaggerated in diabetics if insulin treatment is less than optimal. This abnormal hormonal response may be restored to normal by improved methods of insulin delivery. In normal subjects, regular exercise or training results in enhanced body sensitivity to insulin. This rise in sensitivity may be mediated by augmented insulin binding to receptors. Furthermore, regular exercise may decrease levels of serum triglycerides and low-density lipoprotein cholesterol and increase those of high-density lipoprotein cholesterol. These beneficial effects of training on carbohydrate and lipid metabolism observed in normal subjects may extend to diabetic patients as well.

Blood Glucose↗
PubMed1979

Insulin binding to monocytes in trained athletes: changes in the resting state and after exercise.

Insulin binding to monocytes was examined in trained athletes (long distance runners) and in sedentary control subjects in the resting state and after 3 h of exercise at 40% of maximal aerobic power. At rest, specific binding of 125-I-insulin to monocytes was 69% higher in athletes than in sedentary controls and correlated with maximal aerobic power. The increase in insulin binding was primarily due to an increase in binding capacity. During acute exercise, insulin binding fell by 31% in athletes but rose by 35% in controls. The athletes had a smaller decline in plasma glucose and a lower respiratory exchange ratio during exercise than did controls. We conclude that physical training increases insulin binding to monocytes in the resting state but results in a fall in insulin binding during acute exercise. Changes in insulin binding in athletes thus may account for augmented insulin sensitivity at rest as well as a greater shift from carbohydrate to fat usage during exercise than is observed in untrained controls.

Adult↗
PubMed1978

Is skin preparation necessary before insulin injection?

The effect of routine skin preparation on skin bacterial flora was measured in thirteen insulin-dependent diabetic patients. 5 seconds of skin cleansing of sites on the leg, arm, and abdomen with 70% isopropyl alcohol reduced bacterial counts by 82-91%. During a 3-5 month observation period the subjects omitted skin preparation before insulin injection every other week. More than 1700 insulin injections were given without skin preparation. No signs of local or systemic infection were observed. These results indicate that routine skin preparation with alcohol before insulin injection markedly reduces skin bacterial-counts but may not be necessary to prevent infection at the injection sites.

1-Propanol↗
PubMed1978

Effects of leg exercise on insulin absorption in diabetic patients.

To examine the effects of leg exercise on insulin absorption from various injection sites, 125I-labelled rapid actin insulin (9 units) was injected subcutaneously into the leg, arm or abdomen of patients with insulin-dependent diabetes before one hour of intermittent leg (bicycle) exercise and on a resting, control day. Insulin disappearance from the leg increased by 135 per cent during the first 10 minutes of leg exercise (P less than 0.05) and remained 50 per cent above resting levels after 60 minutes (P less than 0.02). Leg exercise had no effect on insulin disappearance from the arm, but insulin disappearance from the abdomen was reduced during the post-exercise recovery period (P less than 0.02). As compared to leg injection, arm or abdominal injection reduced the hypoglycemic effect of exercise by 57 per cent (P less than 0.02) and 89 per cent (P less than 0.005), respectively. Leg exercise accelerates insulin absorption from the leg. Arm or abdominal injection avoids this acceleration during leg exercise and reduces exercise-induced hypoglycemia.

Abdomen↗