Skeletal muscle inflammation is not responsible for the rapid impairment in adiponectin response with high-fat feeding in rats

Mullen, Kerry Lynn; Tishinsky, Justine M.; Robinson, Lindsay E.; Dyck, David J.

doi:10.1152/ajpregu.00080.2010

Cited by 16 publications

(14 citation statements)

References 47 publications

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“…89 Rats given high-fat diet, which is known to increase the plasma level of free fatty acids, 13,79 developed skeletal muscle adiponectin resistance before insulin resistance 67 and the resistance could not be explained by muscle inflammation. 83 Our analysis revealed a significant correlation between BMI and plasma IL-6 (Figure 4b), but not between BMI and plasma TNFa (Figure 3b). This is consistent with the in vitro observation on adipocytes where larger adipocytes were shown to release more IL-6, but not more TNFa.…”

Section: Lack Of Bmi-adiponectin Association S-m Kuo and MM Halpernmentioning

confidence: 60%

“…Future human studies correlating the plasma level of free fatty acids (and perhaps even the type of free fatty acids 83,84 ) and that of adiponectin are needed to further examine the potential free fatty acid-adiponectin link. Results from correlation studies performed on healthy human studies suggest that such a link exist.…”

Section: Lack Of Bmi-adiponectin Association S-m Kuo and MM Halpernmentioning

confidence: 99%

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Lack of association between body mass index and plasma adiponectin levels in healthy adults

Kuo

2011

Int J Obes

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Objectives: To test the hypothesis that obesity (increase in fat mass) independently affects the level of adipokines: adiponectin, tumor necrosis factor-a (TNFa) and interleukin (IL)-6. Methods: Publications in the past decade reporting adult plasma adiponectin, leptin, TNFa and/or IL-6 levels were compiled. Mean gender-specific values were extracted from studies that included medical screening to confirm physical health (43 groups, total 4852 subjects). Correlation analysis was conducted between adipokine levels and body mass index (BMI), a widely used estimate of adiposity. Results: For healthy lean to obese adults of both genders, no significant correlation between plasma adiponectin and BMI was detected. There was also no gender difference in plasma adiponectin level. In contrast, leptin levels showed a positive correlation with BMI in both genders, and women had significantly higher levels of plasma leptin consistent with a higher percentage of body fat. The proinflammatory cytokine TNFa failed to show correlation with BMI. Although IL-6 showed a positive correlation with BMI in women, the obesity-related increase was very limited. Conclusions: Data analysis based on studies performed on healthy adults did not support the hypothesis that obesity independently affects the plasma level of adiponectin and TNFa. Reported obesity-related changes in plasma adipokine levels may be a consequence of obesity-related metabolic disorders. Future studies are especially needed to understand the homeostasis of adiponectin.

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Section: Lack Of Bmi-adiponectin Association S-m Kuo and MM Halpernmentioning

confidence: 60%

Section: Lack Of Bmi-adiponectin Association S-m Kuo and MM Halpernmentioning

confidence: 99%

Lack of association between body mass index and plasma adiponectin levels in healthy adults

Kuo

2011

Int J Obes

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“…The concept of adiponectin resistance has been mooted and there is strong likelihood that it has important significance in certain pathologies. For example, adiponectin's metabolic effects in human skeletal muscle were blunted in tissue from obese individuals and feeding a diet high in saturated fats attenuated adiponectin-stimulated signalling and fatty acid metabolism in rodent skeletal muscle [53][54][55]. It has been proposed that adiponectin resistance precedes lipid accumulation and further metabolic disturbances induced by lipotoxicity [56].…”

Section: Adiponectin Resistancementioning

confidence: 99%

Adiponectin action in skeletal muscle

Liu¹,

Sweeney²

2014

Best Practice & Research Clinical Endocrinology & Metab

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“…Indeed, strong evidence indicates that adiponectin action is reduced in skeletal muscle from obese versus lean individuals as well as in muscle from rodents fed a diet high in saturated fats [28][29][30]. Thus, it was suggested that adiponectin resistance precedes lipid accumulation and metabolic dysfunction [31].…”

Section: Adiponectin Resistance and Therapeutic Interventionmentioning

confidence: 99%

Skeletal muscle glucose metabolism and inflammation in the development of the metabolic syndrome

Marette

Liu

Sweeney

2014

Rev Endocr Metab Disord

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Insulin resistance and metabolic dysfunction in skeletal muscle play a major role in the development of the metabolic syndrome and type 2 diabetes. Numerous mechanisms have been proposed to explain the pathophysiology of obesity-linked metabolic dysfunction and this review will focus on the contributing role of adiponectin and inflammation. The beneficial effects of adiponectin on both insulin action and inflammation are now well documented and will be reviewed. More recent work provided new insights into adiponectin signaling mechanisms. The development of strategies to mimic adiponectin action holds promise that adiponectin-based compounds may translate into effective therapeutic applications. We will also discussed the novel role of long chain ω-3 PUFA-derived resolution mediators, which in addition to resolving inflammation, can also exert glucoregulatory effects in models of obesity and insulin resistance. We will focus on one resolution mediator, protectin DX (PDX), which was recently shown to act as a muscle interleukin-6 secretagogue. PDX and its isomer PD1 also enhance adiponectin expression and action. Ultimately, it is via a better understanding the molecular mechanisms of action via which inflammation, insulin resistance and metabolic dysfunction occur in skeletal muscle, and also how they crosstalk with each other, that we can generate new and improved therapies for obesity-linked metabolic complications.

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Skeletal muscle inflammation is not responsible for the rapid impairment in adiponectin response with high-fat feeding in rats

Abstract: Mullen KL, Tishinsky JM, Robinson LE, Dyck DJ. Skeletal muscle inflammation is not responsible for the rapid impairment in adiponectin response with high-fat feeding in rats.

Cited by 16 publications

References 47 publications

Lack of association between body mass index and plasma adiponectin levels in healthy adults

Lack of association between body mass index and plasma adiponectin levels in healthy adults

Adiponectin action in skeletal muscle

Skeletal muscle glucose metabolism and inflammation in the development of the metabolic syndrome

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