Tumor necrosis factor-alpha suppresses insulin-induced tyrosine phosphorylation of insulin receptor and its substrates.

Feinstein, Revital; Kanety, Hannah; Papa, Moshe Z.; Lunenfeld, Bruno; Karasik, Avraham

doi:10.1016/s0021-9258(19)74276-8

Cited by 477 publications

(57 citation statements)

References 25 publications

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“…Insulin resistance is an essential prerequisite for diabetogenesis (22). It is thought to represent a chronic inflammatory state (23,24) owing to its induction by tumor necrosis factor-alpha, a proinflammatory cytokine (25,26). Moreover, the presence of inflammation-induced insulin resistance in subjects without diabetes has been documented (27).…”

Section: Discussionmentioning

confidence: 99%

Association Between Elevated C-Reactive Protein Levels and Prediabetes in Adults, Particularly Impaired Glucose Tolerance

Kato

Otsuka

Saiki

et al. 2019

Canadian Journal of Diabetes

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Section: Discussionmentioning

confidence: 99%

Association Between Elevated C-Reactive Protein Levels and Prediabetes in Adults, Particularly Impaired Glucose Tolerance

Kato

Otsuka

Saiki

et al. 2019

Canadian Journal of Diabetes

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“…It has been reported that NFκB contributes to upregulation of proinflammatory cytokines including interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), which cause insulin resistance under inflammatory states (Kern, Ranganathan, Li, Wood, & Ranganathan, 2001). Previous reports have demonstrated that TNF-α directly contributes to impairment of insulin signaling in obese and diabetic animal models (Feinstein, Kanety, Papa, Lunenfeld, & Karasik, 1993;Hotamisligil, 1999;Hotamisligil, Shargill, & Spiegelman, 1993). All of these reports suggest that both ER stress and inflammation cause insulin resistance.…”

mentioning

confidence: 99%

Asprosin attenuates insulin signaling pathway through PKCδ‐activated ER stress and inflammation in skeletal muscle

Jung

Kim

et al. 2019

Journal Cellular Physiology

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It has been reported that asprosin is a novel adipokine which is augmented in mice and humans with type 2 diabetes (T2DM). Asprosin stimulates hepatic gluconeogenesis under fasting conditions. However, the roles of asprosin in inflammation, endoplasmic reticulum (ER) stress, and insulin resistance in skeletal muscle has not been studied. In the currents study, elevated levels of asprosin expression were observed in adipocytes under hyperlipidemic conditions. Treatment of C2C12 myocytes with asprosin-induced ER stress markers (phosphorylated inositol-requiring enzyme 1 and eukaryotic initiation factor 2, and CHOP expression) as well as inflammation markers (interleukin-6 expression, phosphorylated IκB, and nuclear translocated nuclear factor-κβ). Finally, asprosin treatment promoted exacerbation of insulin sensitivity as determined by levels of insulin receptor substrate 1 and Akt phosphorylation as well as glucose uptake. Moreover, treatment of asprosin augmented protein kinase C-δ (PKCδ) phosphorylation and nuclear translocation, but suppressed messenger RNA expression of sarcoplasmic reticulum Ca 2+ ATPase 2b in both C2C12 myocytes and in mouse soleus skeletal muscle. These asprosininduced effects were markedly decreased in small interfering (si) RNA-mediated PKCδ-knockdown in C2C12 myocytes. These results suggest that asprosin results in impairment of insulin sensitivity in skeletal muscle through PKCδ-associated ER stress/inflammation pathways and may be a valuable strategy for management of insulin resistance and T2DM.

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“…This is important because impaired insulin signaling in adipocytes leads to uncontrolled basal lipolysis, which can induce cell death, and also increase the circulating levels of FFAs. In turn, this leads to lipids accumulation in non-adipose organs inducing systemic IR and increasing the risk to develop cardiovascular disease and T2D [ 386 , 387 , 388 ].…”

Section: Brown and Beige Adipose Tissue In Obesity Aging And Metabolic Diseasementioning

confidence: 99%

Thermogenic Fat: Development, Physiological Function, and Therapeutic Potential

Brandão

Poojari

Rabiee

2021

IJMS

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The concerning worldwide increase of obesity and chronic metabolic diseases, such as T2D, dyslipidemia, and cardiovascular disease, motivates further investigations into preventive and alternative therapeutic approaches. Over the past decade, there has been growing evidence that the formation and activation of thermogenic adipocytes (brown and beige) may serve as therapy to treat obesity and its associated diseases owing to its capacity to increase energy expenditure and to modulate circulating lipids and glucose levels. Thus, understanding the molecular mechanism of brown and beige adipocytes formation and activation will facilitate the development of strategies to combat metabolic disorders. Here, we provide a comprehensive overview of pathways and players involved in the development of brown and beige fat, as well as the role of thermogenic adipocytes in energy homeostasis and metabolism. Furthermore, we discuss the alterations in brown and beige adipose tissue function during obesity and explore the therapeutic potential of thermogenic activation to treat metabolic syndrome.

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Tumor necrosis factor-alpha suppresses insulin-induced tyrosine phosphorylation of insulin receptor and its substrates.

Cited by 477 publications

References 25 publications

Association Between Elevated C-Reactive Protein Levels and Prediabetes in Adults, Particularly Impaired Glucose Tolerance

Association Between Elevated C-Reactive Protein Levels and Prediabetes in Adults, Particularly Impaired Glucose Tolerance

Asprosin attenuates insulin signaling pathway through PKCδ‐activated ER stress and inflammation in skeletal muscle

Thermogenic Fat: Development, Physiological Function, and Therapeutic Potential

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