Effects of bariatric surgery on adipokine-induced inflammation and insulin resistance

Zeynep Goktas, Naima Moustaid-Moussa, Chwan-Li Shen, Mallory Boylan, Huanbiao Mo, Shu Wang, Zeynep Goktas, Naima Moustaid-Moussa, Chwan-Li Shen, Mallory Boylan, Huanbiao Mo, Shu Wang

Abstract

Over a third of the US population is obese and at high risk for developing type 2 diabetes, insulin resistance, and other metabolic disorders. Obesity is considered a chronic low-grade inflammatory condition that is primarily attributed to expansion and inflammation of adipose tissues. Indeed, adipocytes produce and secrete numerous proinflammatory and anti-inflammatory cytokines known as adipokines. When the balance of these adipokines is shifted toward higher production of proinflammatory factors, local inflammation within adipose tissues and subsequently systemic inflammation occur. These adipokines including leptin, visfatin, resistin, apelin, vaspin, and retinol binding protein-4 can regulate inflammatory responses and contribute to the pathogenesis of diabetes. These effects are mediated by key inflammatory signaling molecules including activated serine kinases such as c-Jun N-terminal kinase and serine kinases inhibitor κB kinase and insulin signaling molecules including insulin receptor substrates, protein kinase B (PKB, also known as Akt), and nuclear factor kappa B. Bariatric surgery can decrease body weight and improve insulin resistance in morbidly obese subjects. However, despite reports suggesting reduced inflammation and weight-independent effects of bariatric surgery on glucose metabolism, mechanisms behind such improvements are not yet well understood. This review article focuses on some of these novel adipokines and discusses their changes after bariatric surgery and their relationship to insulin resistance, fat mass, inflammation, and glucose homeostasis.

Keywords: adipokines; bariatric surgery; inflammation; insulin resistance; obesity.

Figures

Figure 1
Figure 1
Bariatric surgery procedures; (A) Roux-n-Y Gastric Bypass, (B) Vertical Gastroplasty, (C) Adjustable Gastric Banding.
Figure 2
Figure 2
Effects of TNP-α on insulin signaling pathways. Insulin signals tyrosine phosphorylation of IRS and activates SOS (Son of Sevenless) and the downstream Erk pathway, leading to transcription and growth. In addition, insulin-stimulated Akt phosphorylation leads to glucose uptake, glycogen synthesis, protein synthesis, cell survival and gene transcription. The binding of TNF-α to its receptor increases SOCS-3 expression and activates serine kinases including INK and IKK, which inhibit IRS tyrosine phosphorylation and activation.

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