Seven days of bed rest decrease insulin action on glucose uptake in leg and whole body

Abstract

Impaired glucose tolerance develops in normal humans after short-term bed rest. To elucidate the mechanism, insulin action on whole body glucose uptake rate (WBGUR) and leg glucose uptake rate (LGUR) was measured by sequential euglycemic clamp technique combined with femoral arterial and venous cannulation at insulin concentrations of 10 +/- 1, 18 +/- 1, 37 +/- 2, and 360 +/- 15 microU/ml. Studies were performed before (C) and after (BR) 7 days of strict bed rest. WBGUR was significantly lower after bed rest than before (5.5 +/- 0.4 and 7.2 +/- 0.8 mg.min-1.kg-1, respectively) when insulin was 37 microU/ml. LGUR was even more markedly depressed by bed rest, being 0.6 +/- 0.1, 0.9 +/- 0.2, and 2.8 +/- 0.4 mg.min-1.kg leg-1 (BR) compared with 0.9 +/- 0.1, 1.7 +/- 0.4, and 5.9 +/- 0.5 mg.min-1.kg leg-1 (C) (P less than 0.05) at the three lower insulin concentrations. At these insulin concentrations also, lactate release and glucose oxidation and glycogen storage estimated by indirect calorimetry were lower in the leg after bed rest. At the highest insulin dose WBGUR was similar on BR and C days, while LGUR was lower after bed rest. In conclusion, 7 days of bed rest decrease whole body insulin action, a fact that is explained by decreased insulin action in inactive muscle.

Effects of spinal cord injury on body composition and metabolic profile – Part I

“…77,[79][80][81][82][83][84][85] Excessive body fat, especially in the trunk and lower extremities of those with SCI can lead to an increase in the amount of non-esterified fatty acids due to increased lipolysis (Table 1). This takes place even though increased insulin usually suppresses lipolysis under normal levels of adiposity.…”

“…4,78,82 Likewise, increased fat accumulation in the liver increases insulin resistance and allows increased gluconeogenesis and glucose export out of the liver adding to hyperglycemia which is a precursor of type II DM. 77,[79][80][81][82][83][84][85] Glucose intolerance is found along with hyperinsulemia, demonstrating that the lack of glucose uptake into the muscle and liver cells is not related to the amount of insulin present in the circulation but rather due to factors inhibiting the ability of muscle and liver cells to receive glucose. 77,80,81 Physical inactivity results in decreased muscle GLUT-4 content which is associated with insulin resistance.…”

“…77,[79][80][81][82][83][84][85] Glucose intolerance is found along with hyperinsulemia, demonstrating that the lack of glucose uptake into the muscle and liver cells is not related to the amount of insulin present in the circulation but rather due to factors inhibiting the ability of muscle and liver cells to receive glucose. 77,80,81 Physical inactivity results in decreased muscle GLUT-4 content which is associated with insulin resistance. Physical inactivity due to bed rest for as little as 7 days results in a significant reduction in insulin sensitivity in inactive muscles.…”

“…Physical inactivity due to bed rest for as little as 7 days results in a significant reduction in insulin sensitivity in inactive muscles. 81,82 Another important regulator of the relationship between body composition and metabolic profile after SCI is leptin. [86][87][88] Leptin is a hormone responsible for achieving satiety and maintaining energy homeostasis.…”

Prolonged adaptation to fat-rich diet and training; effects on body fat stores and insulin resistance in man

“…5,6 This improved insulin action and glucose tolerance may primarily be explained by an increase in total muscle GLUT4 content, glycolytic flux capacity and an improved insulin action in skeletal muscle. 5,7 In addition to physical inactivity epidemiological data indicate that an excess in dietary intake and particularly fat intake is considered one of the key factors in the development of glucose intolerance and insulin resistance.…”