Biomedical subjects

W F Nicholson

Publications and source records attributed to W F Nicholson.

8 recordsLinked to original sources

PubMed1984

Levels of blood-bourne factors and cytosol glucocorticoid receptors during the initiation of muscle atrophy in rodent hindlimbs.

When only 1 hindlimb of the adult mouse was immobilized for 13 h, the immobilization-induced failure of insulin to stimulate 2-deoxyglucose uptake was observed in the immobilized soleus muscle. 2-deoxyglucose uptake was unchanged in the contralateral, nonimmobilized muscle. In the rat, protein synthesis rates decreased in the one immobilized limb as compared to rates measured in the contralateral nonimmobilized limb of the same animal. The synthesis rates in the contralateral nonimmobilized limb of a rat with one immobilized limb were not significantly different from rates of muscle protein synthesis observed in rats with no hindlimb immobilization. Specific binding of 3H-dexamethasone, as determined by exchange assay in the gastrocnemius muscle cytosol, increased after 7 days of immobilization, but not after only 6 h of immobilization. Changes in the level of blood-bourne factors or in cytosolic glucocorticoid levels do not by themselves initiate muscle atrophy in immobilized rodent limbs.

Animals↗

PubMed1984

Glucose uptake and glycogen synthesis in muscles from immobilized limbs.

The purposes of this study were to determine whether the defects in glucose metabolism in muscles of immobilized limbs of mice were related to alterations in insulin binding, insulin responsiveness, glucose supply, and insulin activation of glycogen synthase. These were tested by in vitro methodology. A significant lessening in the insulin-induced maximal response of 2-deoxyglucose uptake into the mouse soleus muscle occurred between the 3rd and 8th h of limb immobilization, suggesting a decreased insulin responsiveness. Lack of change in the specific binding of insulin to muscles of 24-h immobilized limbs indicates that a change in insulin receptor number did not play a role in the failure of insulin to stimulate glucose metabolism. It's inability to stimulate glycogen synthesis in muscle from immobilized limbs is due, in part, to a lack of glucose supply to glycogen synthesis and also to the ineffectiveness of insulin to increase the percentage of glycogen synthase in its active form in muscles from 24-h immobilized limbs.

Animals↗

PubMed1982

Insulin resistance for glucose metabolism in disused soleus muscle of mice.

Our hypothesis was that insulin resistance for carbohydrate metabolism develops after a single day of muscular disuse. The immobilization of the mouse hindlimb for 24 h was used to produce muscular disuse (group c). As food intake was voluntarily decreased during the immobilization, two additional groups were used: group A was untreated and ate ad libitum, whereas group B was anesthetized with group C and was fed amounts of food similar to those eaten by group C. Because groups B and C differed only by limb immobilization, group B was used as the reference group. When insulin was present in the incubation media, the rates of 2-deoxyglucose uptake and glycogen synthesis were always significantly decreased in soleus muscles from group C (anesthetized, ate less, immobilized) as compared to group B (anesthetized, pair-fed food that group C ate). Significant interaction between the factors of insulin and muscular disuse for the rates of 2-deoxyglucose uptake and glycogen synthesis support the concept that disuse of skeletal muscle attenuates insulin action. These observations are a direct demonstration of a decrease in insulin responsiveness in skeletal muscle as the result of a single day of muscular inactivity. Because plasma insulin concentrations were significantly lower in groups B and C than in the untreated group, it seems likely that the development of insulin resistance in disused skeletal muscle is independent of plasma insulin levels.

Anesthesia, General↗

PubMed1982