Obesity, macrophage migration inhibitory factor, and weight loss

Church, Timothy S.; Willis, Monte S.; Priest, Elisa L.; LaMonte, Michael J.; Earnest, Conrad P.; Wilkinson, William J.; Wilson, Dalton; Giroir, Brett P.

doi:10.1038/sj.ijo.0802942

Cited by 58 publications

(52 citation statements)

References 15 publications

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“…While introducing IL-17 and IL-23 as additional markers of the inflammatory syndrome that accompanies obesity, our results also confirm earlier reports on the increase in leptin and MIF levels in obese humans. [13][14][15][16][17] Both leptin and MIF are well known for their ability to stimulate secretion of various proinflammatory mediators in different experimental systems, 17,20 the latter being proposed to function as a master controller of systemic inflammation. 20 Moreover, some recent studies indicate that leptin and MIF might also stimulate the expression of IL-17 in human and mouse mononuclear cells, respectively.…”

Section: Discussionmentioning

confidence: 99%

Increased activity of interleukin-23/interleukin-17 proinflammatory axis in obese women

Šumarac-Dumanović

Stevanović

Ljubic³

et al. 2008

Int J Obes

250

187

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Objective: To compare the concentrations of cytokines belonging to Th17 axis (interleukin (IL)-17 and IL-23) and Th1 axis (IL-12 and interferon (IFN)-g) in obese and lean women, and to investigate their relationships with the proinflammatory adipokine leptin, proinflammatory cytokine macrophage migration inhibitory factor (MIF) and anthropometric and metabolic parameters of obesity. Design: Cross-sectional study.

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Section: Discussionmentioning

confidence: 99%

Increased activity of interleukin-23/interleukin-17 proinflammatory axis in obese women

Šumarac-Dumanović

Stevanović

Ljubic³

et al. 2008

Int J Obes

250

187

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“…While most of these studies were performed in the setting of stress, several reports have also documented an association between MIF, obesity, and insulin resistance (IR) in a physiological environment. MIF secretion and serum concentration are increased in obese individuals or in patients with type 2 diabetes (Church et al 2005, Skurk et al 2005, Herder et al 2008, and a polymorphism in the MIF gene promoter has been linked to obesity (Sakaue et al 2006). In addition, several reports have described that an elevated level of MIF is associated with decreased b-cell function and IR (Benigni et al 2000, Church et al 2005, Sakaue et al 2006).…”

Section: Introductionmentioning

confidence: 99%

“…MIF secretion and serum concentration are increased in obese individuals or in patients with type 2 diabetes (Church et al 2005, Skurk et al 2005, Herder et al 2008, and a polymorphism in the MIF gene promoter has been linked to obesity (Sakaue et al 2006). In addition, several reports have described that an elevated level of MIF is associated with decreased b-cell function and IR (Benigni et al 2000, Church et al 2005, Sakaue et al 2006). Finally, in vitro studies have shown that mouse adipocytes treated with MIF, or anti-MIF monoclonal antibody, had altered insulin-mediated glucose transport and insulin receptor signal transduction (Biddinger & Kahn 2006).…”

Section: Introductionmentioning

confidence: 99%

Macrophage migration inhibitory factor deficiency leads to age-dependent impairment of glucose homeostasis in mice

Serre‐Beinier

Toso²,

Morel³

et al. 2010

Journal of Endocrinology

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Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine produced by many cells and tissues including pancreatic b-cells, liver, skeletal muscle, and adipocytes. This study investigates the potential role of MIF in carbohydrate homeostasis in a physiological setting outside of severe inflammation, utilizing Mif knockout (MIFK/K) mice. Compared with wild-type (WT) mice, MIFK/K mice had a lower body weight, from birth until 4 months of age, but subsequently gained weight faster, resulting in a higher body weight at 12 months of age. The lower weight in young mice was related to a higher energy expenditure, and the higher weight in older mice was related to an increased food intake and a higher fat mass. Fasting blood insulin level was higher in MIFK/K mice compared with WT mice at any age. After i.p. glucose injection, the elevation of blood insulin level was higher in MIFK/K mice compared with WT mice, at 2 months of age, but was lower in 12-month-old MIFK/K mice. As a result, the glucose clearance during intraperitoneal glucose tolerance tests was higher in MIFK/K mice compared with WT mice until 4 months of age, and was lower in 12-month-old MIFK/K mice. Insulin resistance was estimated (euglycemic-hyperinsulinemic clamp tests), and the phosphorylation activity of AKT was similar in MIFK/K mice and WT mice. In conclusion, this mouse model provides evidence for the role of MIF in the control of glucose homeostasis.

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“…Furthermore, a weight loss programme in morbidly obese individuals that achieved a 14 . 4 kg reduction in body weight was associated with lower serum MIF concentrations and improved pancreatic b-cell function (119) . It has been demonstrated that patients with T2DM have higher serum MIF (20 .…”

mentioning

confidence: 99%

“…Epidemiological studies implicate MIF in obesity and T2DM (117)(118)(119)(120) . Obese individuals with a BMI of 37 .…”

Section: Macrophage Migration Inhibitory Factormentioning

confidence: 99%

Insights into the role of macrophage migration inhibitory factor in obesity and insulin resistance

et al. 2012

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High-fat diet (HFD)-induced obesity has emerged as a state of chronic low-grade inflammation characterised by a progressive infiltration of immune cells, particularly macrophages, into obese adipose tissue. Adipose tissue macrophages (ATM) present immense plasticity. In early obesity, M2 anti-inflammatory macrophages acquire an M1 pro-inflammatory phenotype. Pro-inflammatory cytokines including TNF-α, IL-6 and IL-1β produced by M1 ATM exacerbate local inflammation promoting insulin resistance (IR), which consequently, can lead to type-2 diabetes mellitus (T2DM). However, the triggers responsible for ATM recruitment and activation are not fully understood. Adipose tissue-derived chemokines are significant players in driving ATM recruitment during obesity. Macrophage migration inhibitory factor (MIF), a chemokine-like inflammatory regulator, is enhanced during obesity and is directly associated with the degree of peripheral IR. This review focuses on the functional role of macrophages in obesity-induced IR and highlights the importance of the unique inflammatory cytokine MIF in propagating obesity-induced inflammation and IR. Given MIF chemotactic properties, MIF may be a primary candidate promoting ATM recruitment during obesity. Manipulating MIF inflammatory activities in obesity, using pharmacological agents or functional foods, may be therapeutically beneficial for the treatment and prevention of obesity-related metabolic diseases.

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Obesity, macrophage migration inhibitory factor, and weight loss

Cited by 58 publications

References 15 publications

Increased activity of interleukin-23/interleukin-17 proinflammatory axis in obese women

Increased activity of interleukin-23/interleukin-17 proinflammatory axis in obese women

Macrophage migration inhibitory factor deficiency leads to age-dependent impairment of glucose homeostasis in mice

Insights into the role of macrophage migration inhibitory factor in obesity and insulin resistance

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