Glucose Uptake and Response to Insulin of the Isolated Rat Diaphragm: The Effect of Denervation

Mg, Buse; Buse, John

doi:10.2337/diab.8.3.218

Cited by 56 publications

(33 citation statements)

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“…Among the possible mechanisms, insulin could conceivably stimulate NO release by a direct, local effect at the vascular endothelium, as previously suggested (13), or indirectly through the activation of a cholinergically mediated stimulation of NO release, as proposed in liver (14). Evidence for cholinergic neurogenic vasodilation in skeletal muscle has been provided in many animal species (15)(16)(17)(18), and interruption of nerve supply to skeletal muscle was shown to result in the development of insulin resistance in the affected muscle (19). Furthermore, applying atropine during the infusion of insulin in anesthetized cats and rats was reported to reduce the effect of insulin on glucose uptake in skeletal muscle (14,20).…”

mentioning

confidence: 78%

Cholinergic Involvement in Vascular and Glucoregulatory Actions of Insulin in Rats

Lévesque

Santuré²,

Pître³

et al. 2006

Diabetes

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This study was designed to test the glucose metabolic and vasodilator actions of insulin in rats and its relation to cholinergic system-dependent mechanisms. The first group of rats had pulsed Doppler flow probes and intravascular catheters implanted to determine blood pressure, heart rate, and regional blood flows. Insulin sensitivity was assessed by the euglycemic-hyperinsulinemic clamp technique carried out in the absence or presence of atropine. The second group of rats was used to determine the cholinergic contribution to in vivo insulin-mediated glucose utilization in individual muscles. Glucose uptake was examined by using [ 3 H]2-deoxy-D-glucose. Muscarinic cholinergic blockade was found to significantly (P ‫؍‬ 0.002) reduce insulin sensitivity and to completely abrogate the renal (P ‫؍‬ 0.008) and hindquarter (P ‫؍‬ 0.02) vasodilator responses to euglycemic infusion of insulin. A significant reduction in insulin-stimulated in vivo glucose uptake was also noted in soleus (P ‫؍‬ 0.006), quadriceps (P ‫؍‬ 0.03), gastrocnemius (P ‫؍‬ 0.02), and extensor digitorum longus (EDL) (P ‫؍‬ 0.001) muscles, when insulin was infused at a rate of 4 mU ⅐ kg ؊1 ⅐ min ؊1 , whereas at the rate of 16 mU ⅐ kg ؊1 ⅐ min ؊1 , a significant reduction in glucose uptake was only observed in EDL (P ‫؍‬ 0.03) and quadriceps (P ‫؍‬ 0.01) muscles. Together, these results demonstrate a potential role for cholinergic involvement with physiological insulin actions in glucose clearance and blood flow regulation in rats. Diabetes 55:398 -404, 2006

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mentioning

confidence: 78%

Cholinergic Involvement in Vascular and Glucoregulatory Actions of Insulin in Rats

Lévesque

Santuré²,

Pître³

et al. 2006

Diabetes

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“…Denervation of skeletal muscle has been shown to cause insulin resistance. 14 Schmalbruch et al 15 studied the morphology of rat soleus muscle denervated for 6 ± 10 months. These investigators found that in chronically denervated muscle, the original ®bers were lost and those surviving were adversely a ected by repeated cycles of regeneration and necrosis.…”

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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“…These interpretations are based on insulin values from 1 fasting time point and may indicate a different outcome had they been based on a 2-hour postprandial glucose load; however, HOMA-IR has been indicated as a valid measure of impaired glucose tolerance in lieu of a glucose challenge (8,89). Insulin resistance in spinal cord dysfunction appears to be directly related to denervation of skeletal muscle (90). There were no SB or SCI subjects with glucose intolerance; however, 8.8% of SB, 30.0% of SCI, and 16.7% of controls had hyperinsulinemia and/or insulin resistance based on fasting insulin concentrations and/or HOMA-IR values, even though known diabetes was an exclusion criterion.…”

Section: Discussionmentioning

confidence: 99%

Metabolic Syndrome in Adolescents With Spinal Cord Dysfunction

Nelson

Widman

Abresch

et al. 2007

The Journal of Spinal Cord Medicine

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Objective: The purpose of this study was to determine the prevalence of components of the metabolic syndrome in adolescents with spinal cord injury (SCI) and spina bifida (SB), and their associations with obesity in subjects with and without SCI and SB.Methods: Fifty-four subjects (20 SCI and 34 SB) age 11 to 20 years with mobility impairments from lower extremity paraparesis were recruited from a hospital-based clinic. Sixty able-bodied subjects who were oversampled for obesity served as controls (CTRL). Subjects were categorized as obese if their percent trunk fat measured by dual x-ray absorptiometry (DXA) was .30.0% for males and .35.0% for females. Ten SCI, 24 SB, and 19 CTRL subjects were classified as obese. Fasting serum samples were collected to determine serum glucose, insulin, and lipid concentrations. Metabolic syndrome was defined as having !3 of the following components: (a) obesity; (b) high-density lipoprotein (HDL) ,45 mg/dL for males; ,50 mg/dL for females; (c) triglycerides !100 mg/dL; (d) systolic or diastolic blood pressure !95th percentile for age/ height/gender, and (e) insulin resistance determined by either fasting serum glucose 100-125 mg/dL; fasting insulin !20lU /mL; or homeostasis model assessment of insulin resistance !4.0.Results: Metabolic syndrome was identified in 32.4% of the SB group and 55% of the SCI group. Metabolic syndrome occurred at a significantly higher frequency in obese subjects (SB ¼ 45.8%, SCI ¼ 100%, CTRL ¼ 63.2%) than nonobese subjects (SB ¼ 0%, SCI ¼ 10%, CTRL ¼ 2.4%). Conclusions:The prevalence of metabolic syndrome in adolescents with SB/SCI is quite high, particularly in obese individuals. These findings have important implications due to the known risks of cardiovascular diseases and diabetes mellitus associated with metabolic syndrome in adults, particularly those with spinal cord dysfunction.

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Glucose Uptake and Response to Insulin of the Isolated Rat Diaphragm: The Effect of Denervation

Cited by 56 publications

References 1 publication

Cholinergic Involvement in Vascular and Glucoregulatory Actions of Insulin in Rats

Cholinergic Involvement in Vascular and Glucoregulatory Actions of Insulin in Rats

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

Metabolic Syndrome in Adolescents With Spinal Cord Dysfunction

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