Insulin stimulation of glucose uptake in skeletal muscles and adipose tissues in vivo is NO dependent

Roy, Denis; Perreault, Mylène; Marette, André

doi:10.1152/ajpendo.1998.274.4.e692

Cited by 200 publications

(191 citation statements)

References 23 publications

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“…Studies with animals and humans supported the hypothesis that the glucose uptake pathway stimulated by NO may be independent of both insulin and muscle contraction (Higaki et al 2001, Henstridge et al 2009). However, other evidence have shown the importance of proper functioning of this system to optimize the insulin-dependent uptake of glucose (Roy et al 1998). In humans, inhibition of NO by L-NMMMA decreased glucose uptake in type 2 diabetics and healthy patients without affecting total blood flow (Bradley et al 1999).…”

Section: Nitric Oxide (No)mentioning

confidence: 99%

General aspects of muscle glucose uptake

Alvim

Cheuhen

Machado

et al. 2015

An. Acad. Bras. Ciênc.

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Glucose uptake in peripheral tissues is dependent on the translocation of GLUT4 glucose transporters to the plasma membrane. Studies have shown the existence of two major signaling pathways that lead to the translocation of GLUT4. The first, and widely investigated, is the insulin activated signaling pathway through insulin receptor substrate-1 and phosphatidylinositol 3-kinase. The second is the insulin-independent signaling pathway, which is activated by contractions. Individuals with type 2 diabetes mellitus have reduced insulin-stimulated glucose uptake in skeletal muscle due to the phenomenon of insulin resistance. However, those individuals have normal glucose uptake during exercise. In this context, physical exercise is one of the most important interventions that stimulates glucose uptake by insulin-independent pathways, and the main molecules involved are adenosine monophosphate-activated protein kinase, nitric oxide, bradykinin, AKT, reactive oxygen species and calcium. In this review, our main aims were to highlight the different glucose uptake pathways and to report the effects of physical exercise, diet and drugs on their functioning. Lastly, with the better understanding of these pathways, it would be possible to assess, exactly and molecularly, the importance of physical exercise and diet on glucose homeostasis. Furthermore, it would be possible to assess the action of drugs that might optimize glucose uptake and consequently be an important step in controlling the blood glucose levels in diabetic patients, in addition to being important to clarify some pathways that justify the development of drugs capable of mimicking the contraction pathway.

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Section: Nitric Oxide (No)mentioning

confidence: 99%

General aspects of muscle glucose uptake

Alvim

Cheuhen

Machado

et al. 2015

An. Acad. Bras. Ciênc.

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“…Whereas one report suggests that eNOS is also expressed in muscle cells [27], most studies failed to detect eNOS in these cells by immunocytochemistry [25,35,36], thus suggesting that the impaired eNOS expression in diabetic rats is mainly localised to the endothelial cells of the muscle vasculature. Because vascular NO production is important for the stimulatory action of insulin on skeletal muscle glucose uptake in vivo [17], the present data suggest that impaired muscle NOS activity is responsible, at least in part, for the lack of insulin-mediated glucose disposal in skeletal muscle of diabetic rats [5].…”

Section: Discussionmentioning

confidence: 64%

“…Nitric oxide synthase activity was quantified by the conversion of [ 3 H]-l-arginine to [ 3 H]-l-citrulline, with minor modifications [12,17]. Briefly, aliquots of the homogenates (100±200 mg proteins) were incubated in 50 mmol/l HEPES (pH 7.4) with 24 mmol/l [ 3 H]-l-arginine (0.1 mCi/tube), 120 mmol/l NADPH, 60 mmol/l l-valine, 12 mmol/l l-citrulline, 1.2 mmol/l MgCl 2 , 0.2 mmol/l CaCl 2 , 10 mg/ml calmodulin, 3 mmol/l BH4, 1 mmol/l flavin adenine dinucleotide (FAD) and 1 mmol/l flavin mononucleotide (FMN).…”

Section: Skeletal Muscle Fractionationmentioning

confidence: 99%

“…Endothelial cell eNOS is thought to play a critical part in modulating muscle glucose utilisation by mediating the haemodynamic action of insulin on the muscle vasculature, thus providing an increased supply of glucose and insulin to the muscle fibres [14±16]. This concept has been recently supported by our observation that the NOS inhibitor N G -nitro-l-arginine methyl ester (l-NAME) greatly reduces insulin-stimulated glucose uptake in muscle when given to rats in vivo during an hyperinsulinaemic-euglycaemic clamp [17].…”

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confidence: 99%

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Mechanism of impaired nitric oxide synthase activity in skeletal muscle of streptozotocin-induced diabetic rats

2000

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Type I (insulin-dependent) diabetes mellitus is characterised by pronounced insulin resistance for glucose disposal in skeletal muscle [1,2]. This metabolic impairment is at least in part related to a post-insulin signalling defect in the expression and translocation of GLUT4 glucose transporters to the muscle cell surface [3±5]. The lack of insulin action on glucose metabolism in muscle of people with Type I diabetes could also be explained by an impaired vasodilatory effect of insulin on the muscle vasculature [2], although this impairment has not been confirmed in a more recent study [1]. Several studies have shown that endothelium-dependent relaxation is altered in Abstract Aims/hypothesis. The aims of our study were to investigate whether nitric oxide synthase (NOS) activity is impaired in skeletal muscle of insulin-deficient [Type I (insulin-dependent)] diabetic rats and if the case, to determine the mechanism of NOS dysregulation in this disorder. Methods. Rats were rendered diabetic by streptozotocin injection (65 mg/kg, i. v.) and NOS activity and expression in gastrocnemius muscles were studied 1, 2, 3 or 4 weeks after diabetes induction. Results. The diabetic state was associated with a progressive reduction (down to 42 % of control values after 4 weeks) in muscle NOS activity compared with control rats. Using reverse transcriptase-polymerase chain reaction, we could not detect statistically significant changes in the expression of either neuronal NOS (nNOS) or endothelial NOS (eNOS) mRNAs in diabetic muscle. The contents of nNOS and eNOS protein were, however, progressively reduced in muscle homogenates of diabetic rats and these alterations were prevented by insulin treatment. Subcellular fractionation of skeletal muscle showed that both nNOS and eNOS proteins are mainly localised to the plasma membrane with lower abundance in T-tubules and not detectable in sarcoplasmic reticulum-enriched fractions. After 1 week of diabetes, eNOS protein content was decreased only in the plasma membrane whereas nNOS protein abundance was not affected at this time. Neither the expression nor the interaction of caveolin-1 and caveolin-3 with NOS enzymes was found to be altered in muscle of diabetic rats. Conclusion/interpretation. These results show that skeletal muscle NOS activity is impaired during the progression of insulin-deficient diabetes and reduced NOS activity is associated with a decreased abundance of both nNOS and eNOS proteins, which appears to involve post-transcriptional mechanisms.

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“…5,13,14,50 It has been suggested that hyperuricemia inhibits nitric oxide availability and decreases insulin-mediated glucose uptake in skeletal muscle and may, therefore, have a role in the development of the metabolic syndrome. 51,52 Other studies have suggested that hyperinsulinemia, a consequence of the metabolic syndrome, enhances the tubular reabsorption of uric acid and that this occurs concurrently with a decrease in sodium and potassium excretion, leading to elevated BP. 53 In both instances, the association between abdominal obesity and high BP is mediated by hyperinsulinemia, 16 which is consistent with the notion of a common exposure to hyperinsulinemia (and obesity) in the relation between SUA and BP.…”

Section: Discussionmentioning

confidence: 99%

Impact of different adiposity measures on the relation between serum uric acid and blood pressure in young adults

et al. 2011

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Serum uric acid (SUA) concentration is independently associated with blood pressure (BP) in adults. We examined this association in young adults at an age where anti-hypertension treatment, other potential confounding factors and co-morbidity are unlikely to occur. We assessed BP, anthropometric variables including weight, height, waist circumference (WC), body fat percent (using bioimpedance), lifestyle behaviors, SUA and blood lipids in 549 participants aged 19-20 years from a population-based cohort study (Seychelles Child Development Study). Mean (s.d.) SUA was higher in males than females, 0.33 (0.08) and 0.24 (0.07) mmol l À1 , respectively. Body mass index (BMI) was higher in females than males but BP was markedly higher in males than in females. SUA was associated with both systolic and diastolic BP. However, the magnitude of the linear regression coefficients relating BP and SUA decreased by up to 50% upon adjustment for BMI, WC or body fat percent. The association between SUA and BP was not altered upon further adjustment for alcohol intake, smoking, triglycerides or renal function. In fully adjusted models, SUA remained associated with BP (Po0.05) in females. In conclusion, adiposity substantially decreased the association between SUA and BP in young adults, and BP was independently associated with SUA in females. These findings suggest a role of adiposity in the link between hyperuricemia and hypertension.

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Insulin stimulation of glucose uptake in skeletal muscles and adipose tissues in vivo is NO dependent

Cited by 200 publications

References 23 publications

General aspects of muscle glucose uptake

General aspects of muscle glucose uptake

Mechanism of impaired nitric oxide synthase activity in skeletal muscle of streptozotocin-induced diabetic rats

Impact of different adiposity measures on the relation between serum uric acid and blood pressure in young adults

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