Insulin resistance of denervated rat muscle: a model for impaired receptor-function coupling

Burant, Charles F.; Lemmon, Sandra K.; Treutelaar, Mary K.; Buse, Maria G.

doi:10.1152/ajpendo.1984.247.5.e657

Cited by 59 publications

(64 citation statements)

References 26 publications

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“…The increase in basal glucose utilization observed in the present study may be an effect of denervation as a comparable effect has been described in rat diaphragm after denervation [23,24]. The in vivo effect of denervation (24 h) to decrease substantially insulin-induced glycogen synthesis in soleus [25] and diaphragm [24] was not seen in vitro in the present study. Factors in addition to denervation per se may therefore be involved in vivo.…”

Section: Resultssupporting

confidence: 81%

Long term culture of rat soleus muscle in vitro

et al. 1990

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Rat soleus muscle strips cultured for 24 h in medium 199 were well preserved in terms of electron microscopy; ATP and creatine phosphate concentrations; rates of glucose utilization, glycogen and protein synthesis, and effects of insulin thereon. Culture led to modest changes in fluid spaces and intracellular (K+); increased basal glucose utilization up to two-fold; had no effect on the maximum response to insulin; and had no effect on sensitivity to insulin except in the presence of adenosine deaminase. Thus in vitro neither denervation nor absence of insulin had any marked effects in 24 h to decrease responses to insulin.

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Section: Resultssupporting

confidence: 81%

Long term culture of rat soleus muscle in vitro

et al. 1990

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“…The glycogen was precipitated by the sequential addition of 100 l of 2 M Na 2 SO 4 and 1 ml EtOH at Ϫ 20 Њ C for 16 h. The pellet was collected and washed twice with 1 ml KOH and 1 ml of EtOH and hydrolyzed in 0.5 ml 4 N H 2 SO 4 at 100 Њ C for 1 h. The solution was neutralized and glucose determined by the glucose oxidase method (22).…”

Section: St Louis Mo] and Triglycerides/gb [Boehringer Mannheim])mentioning

confidence: 99%

Troglitazone action is independent of adipose tissue.

et al. 1997

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We have investigated the antidiabetic action of troglitazone in aP2/DTA mice, whose white and brown fat was virtually eliminated by fat-specific expression of diphtheria toxin A chain. aP2/DTA mice had markedly suppressed serum leptin levels and were hyperphagic, but did not gain excess weight. aP2/DTA mice fed a control diet were hyperlipidemic, hyperglycemic, and had hyperinsulinemia indicative of insulin-resistant diabetes. Treatment with troglitazone alleviated the hyperglycemia, normalized the tolerance to intraperitoneally injected glucose, and significantly decreased elevated insulin levels. Troglitazone also markedly decreased the serum levels of cholesterol, triglycerides, and free fatty acids both in wild-type and aP2/DTA mice. The decrease in serum triglycerides in aP2/DTA mice was due to a marked reduction in VLDL-and LDL-associated triglyceride. In skeletal muscle, triglyceride levels were decreased in aP2/DTA mice compared with controls, but glycogen levels were increased. Troglitazone treatment decreased skeletal muscle, but not hepatic triglyceride and increased hepatic and muscle glycogen content in wild-type mice. Troglitazone decreased muscle glycogen content in aP2/DTA mice without affecting muscle triglyceride levels. The levels of peroxisomal proliferator-activated receptor ␥ mRNA in liver increased slightly in aP2/DTA mice and were not changed by troglitazone treatment. The results demonstrate that insulin resistance and diabetes can occur in animals without significant adipose deposits. Furthermore, troglitazone can alter glucose and lipid metabolism independent of its effects on adipose tissue. ( J. Clin. Invest. 1997. 100:2900-2908.)

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“…16 Electrical stimulation has been shown to improve muscle ®ber structure and function. 15,17,18 In animal models, investigators have reported the deleterious e ect of denervation on postreceptor insulin action, 19 exercise-induced glucose uptake, 20 insulin receptor binding, 21,22 receptor phosphorylation, 21 and the glucose transporter protein (GLUT-4). 23 ± 25 In a recent study, 26 individuals with tetraplegia were found to have a marked reduction in whole body glucose transport that appeared to be due to a proportional reduction in muscle mass.…”

Section: Determinants Of Insulin Resistancementioning

confidence: 99%

Risk factors for atherogenesis and cardiovascular autonomic function in persons with spinal cord injury

et al. 1999

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Persons with spinal cord injury (SCI) have been recognized to have several metabolic changes that adversely impact their risk for cardiovascular disease. An increased prevalence of disorders of carbohydrate metabolism and dyslipidemia may be related predominantly to paralysis with immobilization and associated loss of lean body tissue and gain in relative adiposity. Studies have reported an increased risk of vascular disease in those with SCI. As such, an understanding of the constellation of carbohydrate and lipid changes that occur after SCI is relevant to the clinical practice of medicine in this population. Oral glucose tolerance testing and associated studiesImpaired glucose tolerance and diabetes mellitus are more prevalent in individuals with SCI than in those who are able-bodied. 1 ± 4 In most of the individuals with SCI and abnormal carbohydrate tolerance, resistance to insulin mediation of glucose uptake by peripheral tissues may be demonstrable. In the presence of insulin resistance, the normal homeostatic response to glucose challenge is increased pancreatic b-cell secretion of insulin. If the compensatory response of the pancreas is insu cient to control the serum glucose concentration, worsening of carbohydrate tolerance will ensue.Bauman et al 3 performed a 75 g oral glucose tolerance test in 100 male veterans with SCI and in 50 able-bodied veteran controls. According to criteria established by the World Health Organization, 5 22% of those with SCI were diabetic whereas only 6% of the control group were diabetic. Eighty-two per cent of the controls had normal oral glucose tolerance, compared with 38% of those with quadriplegia and 50% of those with paraplegia. Subjects with SCI had signi®cantly higher mean plasma glucose and insulin values at several points during the oral glucose tolerance test when compared with controls ( Figure 1). In subgroups, determinants of insulin sensitivity were measured: per cent lean body mass, per cent fat mass, and cardiopulmonary ®tness. Values for insulin sensitivity were linearly related with those of ®tness (VO 2 max) determined from a progressive incremental upper-body exercise stress test. Insulin sensitivity was suggestively correlated with lean body mass, and negatively correlated with body fat. Thus, in a relatively small subgroup of untrained subjects with paraplegia, the strongest determinant of insulin sensitivity was cardiopulmonary ®tness.In 201 non-veteran subjects with SCI, Bauman et al 2 studied the relationship of oral carbohydrate tolerance after a 75 g glucose load to several variables, including level and completeness of lesion, gender, ethnicity, age, duration of injury, and anthropometric measures. Of the total group, 27 (13%) had diabetes mellitus and 56 (29%) had impaired glucose tolerance. 2,6 The subjects with complete tetraplegia had sign®cantly worse carbohydrate tolerance (Figure 2) and were more frequently classi®ed with a disorder of carbohydrate tolerance than the other neurological de®cit subgroups. 2 There were no signi®cant gend...

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Insulin resistance of denervated rat muscle: a model for impaired receptor-function coupling

Cited by 59 publications

References 26 publications

Long term culture of rat soleus muscle in vitro

Long term culture of rat soleus muscle in vitro

Troglitazone action is independent of adipose tissue.

Risk factors for atherogenesis and cardiovascular autonomic function in persons with spinal cord injury

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