Effects of long-term caloric restriction on glucose homeostasis and on the first steps of the insulin signaling system in skeletal muscle of normal and Ames dwarf (Prop1df/Prop1df) mice

Argentino, Danila P.; Dominici, Fernando Pablo; Muñoz, Marina Cecilia; Al-Regaiey, Khalid; Bartke, Andrzej; Turyn, Daniel

doi:10.1016/j.exger.2004.09.005

Cited by 30 publications

(35 citation statements)

References 33 publications

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“…Previous research that quantified insulin receptors in skeletal muscle using various methods, including Western blotting (2)(3)(4)42) and insulin receptor binding (7,14), has usually found no effect of CR, consistent with the present results, although Wang et al (39) reported increased insulin receptor binding in rat skeletal muscle after CR. Two studies have indicated that insulin receptor tyrosine phosphorylation can be increased by CR in muscle (3,18), whereas an equal number of studies have not found this effect of CR (2,4).…”

Section: Discussionsupporting

confidence: 81%

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In vitro simulation of calorie restriction-induced decline in glucose and insulin leads to increased insulin-stimulated glucose transport in rat skeletal muscle

Arias¹,

Cartee²

2007

American Journal of Physiology-Endocrinology and Metabolism

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Arias EB, Cartee GD. In vitro simulation of calorie restrictioninduced decline in glucose and insulin leads to increased insulinstimulated glucose transport in rat skeletal muscle. Am J Physiol Endocrinol Metab 293: E1782-E1788, 2007. First published October 9, 2007; doi:10.1152/ajpendo.00531.2007.-In vivo calorie restriction [CR; consuming 60% of ad libitum (AL) intake] induces elevated insulin-stimulated glucose transport (GT) in skeletal muscle. The mechanisms triggering this adaptation are unknown. The aim of this study was to determine whether physiological reductions in extracellular glucose and/or insulin, similar to those found with in vivo CR, were sufficient to elevate GT in isolated muscles. Epitrochlearis muscles dissected from rats were incubated for 24 h in media with glucose (8 mM) and insulin (80 U/ml) at levels similar to plasma values of AL-fed rats and compared with muscles incubated with glucose (5.5 mM) and/or insulin (20 U/ml) at levels similar to plasma values of CR rats. Muscles incubated with CR levels of glucose and insulin for 24 h had a subsequently greater (P Ͻ 0.005) GT with 80 U/ml insulin and 8 mM [3 H]-3-O-methylglucose but unchanged GT without insulin. Reducing only glucose or insulin for 24 h or both glucose and insulin for 6 h did not induce altered GT. Increased GT after 24-h incubation with CR levels of glucose and insulin was not attributable to increased insulin receptor tyrosine phosphorylation, Akt serine phosphorylation, or Akt substrate of 160 kDa phosphorylation. Nor did 24-h incubation with CR levels of glucose and insulin alter the abundance of insulin receptor, insulin receptor substrate-1, GLUT1, or GLUT4 proteins. These results provide the proof of principle that reductions in extracellular glucose and insulin, similar to in vivo CR, are sufficient to induce an increase in insulin-stimulated glucose transport comparable to the increase found with in vivo CR. diet restriction; insulin signaling; GLUT4; Akt; Akt substrate of 160 kDa ALTERED SKELETAL MUSCLE GLUCOSE transport can contribute to important systemic changes in glucose homeostasis. For example, skeletal muscle insulin resistance for glucose uptake is an early and essential defect for the subsequent development of the metabolic syndrome and type 2 diabetes mellitus (19,20). Previous studies have demonstrated that prior exposure of skeletal muscle to large changes in extracellular glucose and insulin concentrations over a period of hours can lead to altered glucose transport. However, only a few studies have characterized the effects of moderate physiological changes in glucose on glucose transport. In cultured myocytes, increasing glucose from ϳ5 to ϳ8 -10 mM for 24 h did not markedly reduce glucose transport (31, 38). In isolated rat soleus muscles, there was also little difference in glucose uptake without insulin after 3 h of incubation with ϳ5 compared with ϳ8 mM glucose (38), but it is possible that a more prolonged incubation would reveal an effect in this range of glucose concentrations.Knowledge i...

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Section: Discussionsupporting

confidence: 81%

“…Two studies have indicated that insulin receptor tyrosine phosphorylation can be increased by CR in muscle (3,18), whereas an equal number of studies have not found this effect of CR (2,4). In addition, Zhu et al (42,43) found that CR led to increased insulin receptor tyrosine phosphorylation in muscle from old, but not young, rats.…”

Section: Discussionmentioning

confidence: 98%

In vitro simulation of calorie restriction-induced decline in glucose and insulin leads to increased insulin-stimulated glucose transport in rat skeletal muscle

Arias¹,

Cartee²

2007

American Journal of Physiology-Endocrinology and Metabolism

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“…Indeed, studies using the PI3K inhibitor, wortmannin (6), and mice with KO of Akt2 (3), reveal that PI3K and Akt2 are essential for the ability of brief CR to enhance skeletal muscle insulin sensitivity. In contrast, CR does not appear to augment insulin action upstream of PI3K at the level of the IR or Irs1 in response to submaximal insulin (9) but has been shown to enhance IR-Irs1 activation in response to supraphysiological insulin stimulation (8,9,11,23), although this is not a universal finding (24,25). In addition, mice with KO of Irs1 exhibit the expected increase in skeletal muscle insulin sensitivity after CR (26).…”

Section: Discussionmentioning

confidence: 78%

Sirt1 enhances skeletal muscle insulin sensitivity in mice during caloric restriction

Schenk¹,

McCurdy²,

Philp³

et al. 2011

J. Clin. Invest.

169

186

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Skeletal muscle insulin resistance is a key component of the etiology of type 2 diabetes. Caloric restriction (CR) enhances the sensitivity of skeletal muscle to insulin. However, the molecular signals within skeletal muscle linking CR to improved insulin action remain largely unknown. Recently, the mammalian ortholog of Sir2, sirtuin 1 (Sirt1), has been identified as a potential transducer of perturbations in cellular energy flux into subsequent metabolic adaptations, including modulation of skeletal muscle insulin action. Here, we have demonstrated that CR increases Sirt1 deacetylase activity in skeletal muscle in mice, in parallel with enhanced insulin-stimulated phosphoinositide 3-kinase (PI3K) signaling and glucose uptake. These adaptations in skeletal muscle insulin action were completely abrogated in mice lacking Sirt1 deacetylase activity. Mechanistically, Sirt1 was found to be required for the deacetylation and inactivation of the transcription factor Stat3 during CR, which resulted in decreased gene and protein expression of the p55α/p50α subunits of PI3K, thereby promoting more efficient PI3K signaling during insulin stimulation. Thus, these data demonstrate that Sirt1 is an integral signaling node in skeletal muscle linking CR to improved insulin action, primarily via modulation of PI3K signaling.

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“…CR uncouples insulin/IGF-I signaling to FoxO factors by markedly reducing plasma IGF-I and insulin levels in rats (Sonntag et al, 1999). These decreases in circulating insulin/IGF-I levels result in decreased Akt phosphorylation in liver and decreased PI3K expression in muscle (Argentino et al, 2005). In addition there is a compensatory increase in the expression of FoxO family members by fasting (Imae et al, 2003;Furuyama et al, 2003) or CR Tsuchiya et al, 2004).…”

Section: Foxo Transcription Factorsmentioning

confidence: 90%

Caloric restriction and intermittent fasting: Two potential diets for successful brain aging

Martin

Mattson

Maudsley

2006

Ageing Research Reviews

323

221

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The vulnerability of the nervous system to advancing age is all too often manifest in neurodegenerative disorders such as Alzheimer's and Parkinson's diseases. In this review article we describe evidence suggesting that two dietary interventions, caloric restriction (CR) and intermittent fasting (IF), can prolong the health-span of the nervous system by impinging upon fundamental metabolic and cellular signaling pathways that regulate life-span. CR and IF affect energy and oxygen radical metabolism, and cellular stress response systems, in ways that protect neurons against genetic and environmental factors to which they would otherwise succumb during aging. There are multiple interactive pathways and molecular mechanisms by which CR and IF benefit neurons including those involving insulin-like signaling, FoxO transcription factors, sirtuins and peroxisome proliferatoractivated receptors. These pathways stimulate the production of protein chaperones, neurotrophic factors and antioxidant enzymes, all of which help cells cope with stress and resist disease. A better understanding of the impact of CR and IF on the aging nervous system will likely lead to novel approaches for preventing and treating neurodegenerative disorders.

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Effects of long-term caloric restriction on glucose homeostasis and on the first steps of the insulin signaling system in skeletal muscle of normal and Ames dwarf (Prop1df/Prop1df) mice

Cited by 30 publications

References 33 publications

In vitro simulation of calorie restriction-induced decline in glucose and insulin leads to increased insulin-stimulated glucose transport in rat skeletal muscle

In vitro simulation of calorie restriction-induced decline in glucose and insulin leads to increased insulin-stimulated glucose transport in rat skeletal muscle

Sirt1 enhances skeletal muscle insulin sensitivity in mice during caloric restriction

Caloric restriction and intermittent fasting: Two potential diets for successful brain aging

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