Adiponectin Resistance Precedes The Accumulation Of Skeletal Muscle Lipids And Insulin Resistance In High-fat Fed Rats.

Mullen, Kerry Lynn; Pritchard, Janet M.; Ritchie, Ian R. W.; Snook, Laelie A.; Chabowski, Adrian; Bonen, Arend; Wright, David C.; Dyck, David J.

doi:10.1249/01.mss.0000353381.96933.38

Cited by 5 publications

(23 citation statements)

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“…Adiponectin resistance, initially described in obesity and conditions associated with insulin resistance, is thought to be partly due to of down-regulation of the adiponectin receptor AdipoR1. 82,88 This hypothesis is supported by a number of studies in humans and rodents and laboratory work with in vitro cell lines. 62,[88][89][90][91][92][93] Molecular cloning and knock-down of AdipoR1 have improved understanding of the physiological and pathological actions of AdipoR1 and its role in adiponectin resistance.…”

Section: New Insights Originating From Adipor1mentioning

confidence: 89%

“…76 As such, López Teros et al 81 studied insulin levels and muscle mass in a cohort study of 147 older adults during an average follow-up period of 4.6 years and demonstrated that hyperinsulinemia is a significant risk marker of appendicular skeletal muscle wasting at older age. Still, it should be noted that Mullen et al 82 found evidence for adiponectin resistance to emerge prior to the initiation of skeletal muscle insulin resistance in high-fat fed rats. The interplay between insulin and adiponectin resistance is discussed in more detail below.…”

Section: Adiponectin Resistance and Insulin Resistancementioning

confidence: 98%

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Adiponectin resistance in skeletal muscle: pathophysiological implications in chronic heart failure

Sente

Berendoncks

Hoymans

et al. 2015

J cachexia sarcopenia muscle

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Skeletal muscle wasting is a common complication of chronic heart failure (CHF) and linked to poor patient prognosis. In recent years, adiponectin was postulated to be centrally involved in CHF‐associated metabolic failure and muscle wasting. This review discusses current knowledge on the role of adiponectin in CHF. Particular emphasis will be given to the complex interaction mechanisms and the intracellular pathways underlying adiponectin resistance in skeletal muscle of CHF patients. In this review, we propose that the resistance process is multifactorial, integrating abnormalities emanating from insulin signalling, mitochondrial biogenesis, and ceramide metabolism.

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Section: New Insights Originating From Adipor1mentioning

confidence: 89%

Section: Adiponectin Resistance and Insulin Resistancementioning

confidence: 98%

Adiponectin resistance in skeletal muscle: pathophysiological implications in chronic heart failure

Sente

Berendoncks

Hoymans

et al. 2015

J cachexia sarcopenia muscle

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show abstract

“…Adiponectin resistance is well recognized in liver, adipose tissue and muscle, and is closely associated with insulin resistance. Indeed, gAd responsiveness is significantly reduced in skeletal muscle from obese/ diabetic patients (Bruce et al 2005;Chen et al 2005) and animals fed a HFD (Mullen et al 2007(Mullen et al , 2009), as well as in liver tissue from insulin receptor transgenic/knockout mice (Lin et al 2007) or heart tissue from HFD-induced diabetic mice (Yi et al 2011). Reduced vascular responsiveness to adiponectin has also been reported in the aorta from hyperlipidaemic rats (Li et al 2007) and resistance arteries of Zucker diabetic fatty rats (Schmid et al 2011).…”

Section: Discussionmentioning

confidence: 99%

Globular adiponectin ameliorates metabolic insulin resistance via AMPK‐mediated restoration of microvascular insulin responses

Zhao

et al. 2015

The Journal of Physiology

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Key pointsr Adiponectin is an adipokine with anti-inflammatory and anti-diabetic properties. Hypoadiponectinaemia is closely associated with endothelial dysfunction and insulin resistance in obesity and diabetes.r Insulin resistance is present in muscle microvasculature and this may contribute to decreased insulin delivery to, and action in, muscle.r In this study we examined whether adiponectin ameliorates metabolic insulin resistance by affecting muscle microvascular recruitment.r We demonstrated that a high-fat diet induces vascular adiponectin and insulin resistance but globular adiponectin administration can restore vascular insulin responses and improve insulin's metabolic action via an AMPK-and nitric oxide-dependent mechanism.r This suggests that globular adiponectin might have a therapeutic potential for improving insulin resistance and preventing cardiovascular complications in patients with diabetes via modulation of microvascular insulin responses.Abstract Hypoadiponectinaemia is closely associated with endothelial dysfunction and insulin resistance, and microvasculature plays a critical role in the regulation of insulin action in muscle. Here we tested whether adiponectin replenishment could improve metabolic insulin sensitivity in male rats fed a high-fat diet (HFD) via the modulation of microvascular insulin responses. Male Sprague-Dawley rats were fed either a HFD or low-fat diet (LFD) for 4 weeks. Small resistance artery myograph changes in tension, muscle microvascular recruitment and metabolic response to insulin were determined. Compared with rats fed a LFD, HFD feeding abolished the vasodilatory actions of globular adiponectin (gAd) and insulin on pre-constricted distal saphenous arteries. Pretreatment with gAd improved insulin responses in arterioles isolated from HFD rats, which was blocked by AMP-activated protein kinase (AMPK) inhibition. Similarly, HFD abolished microvascular responses to either gAd or insulin and decreased insulin-stimulated glucose disposal by ß60%. However, supplementing gAd fully rescued insulin's microvascular action and significantly improved the metabolic responses to insulin in HFD male rats and these actions were abolished by inhibition of either AMPK or nitric oxide production. We conclude that HFD induces vascular adiponectin and insulin resistance but gAd administration can restore vascular insulin responses and improve insulin's metabolic action via an AMPK-and nitric oxide-dependent mechanism in male rats.

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“…In mice, adiponectin treatment lowers glycaemia and improves insulin sensitivity (Yamauchi et al 2001). This effect is largely attributed to the increased phosphorylation of AMP-activated protein kinase (AMPK) and subsequent increase in fatty acid (FA) oxidation and glucose uptake (Yamauchi et al 2002;Bruce et al 2005;Mullen et al 2009).…”

Section: Introductionmentioning

confidence: 99%

Adiponectin is sufficient, but not required, for exercise‐induced increases in the expression of skeletal muscle mitochondrial enzymes

Ritchie

MacDonald

Wright

et al. 2014

The Journal of Physiology

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Key pointsr Adiponectin is a regulator of skeletal muscle mitochondrial biogenesis. Previous research using the ob/ob mouse (leptin deficient, low adiponectin) has suggested that the presence of adipokines, including adiponectin, is necessary for exercise-induced increases in mitochondrial content.r In the current study, we examined the importance of adiponectin as a regulator of skeletal muscle mitochondrial content in response to exercise by comparing wildtype and adiponectin deficient mice.r Adiponectin deficient mice showed no differences in resting V O 2 , RER, or time to exhaustion during exercise when compared to wildtype mice. There were no differences in various protein markers of mitochondrial content.r A single bout of treadmill running increased the mRNA expression of mitochondrial proteins similarly in wildtype and adiponectin deficient mice. Chronic exercise (8 weeks) also increased the protein content of mitochondrial markers similarly in wildtype and adiponectin deficient mice.r We conclude that Ad is not required for exercise-induced increases in muscle mitochondrial proteins.Abstract Adiponectin (Ad) has been proposed to be a regulator of mitochondrial biogenesis in skeletal muscle, and necessary for exercise-induced increases in mitochondrial content. We first confirmed that Ad could acutely increase the expression of mitochondrial proteins during a 10 h incubation in isolated soleus and extensor digitorum longus (EDL) muscles. Next, we further examined the role of Ad as a regulator of mitochondrial content using Ad knockout (AdKO) mice. The AdKO animals showed no differences in resting V O 2 , respiratory exchange ratio, or in time to exhaustion during exercise when compared to wild-type (WT) mice. There was a reduction in resting palmitate oxidation in isolated soleus from AdKO animals (−23%, P < 0.05) but not EDL, and 5-aminoimidazole-4-carboxamide (AICAR)-stimulated palmitate oxidation was similar in both genotypes regardless of muscle. There were no differences in protein markers of mitochondrial content (COX4, CORE1, CS, PDHE1α) in red and white gastrocnemius between WT and AdKO animals. A single bout of treadmill running increased the phosphorylation of AMP-activated protein kinase (AMPK) and the mRNA expression of mitochondrial proteins in red and white gastrocnemius in both WT and AdKO animals, with no differences between genotypes. Finally, 8 weeks of chronic exercise training increased the protein content of mitochondrial markers similarly (ß25-35%) in red gastrocnemius from both WT and AdKO mice. Collectively, our results demonstrate that the absence of Ad is not accompanied

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Adiponectin Resistance Precedes The Accumulation Of Skeletal Muscle Lipids And Insulin Resistance In High-fat Fed Rats.

Cited by 5 publications

References 0 publications

Adiponectin resistance in skeletal muscle: pathophysiological implications in chronic heart failure

Adiponectin resistance in skeletal muscle: pathophysiological implications in chronic heart failure

Globular adiponectin ameliorates metabolic insulin resistance via AMPK‐mediated restoration of microvascular insulin responses

Adiponectin is sufficient, but not required, for exercise‐induced increases in the expression of skeletal muscle mitochondrial enzymes

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