Expression of resistin in the adipose tissue is modulatedby various factors including peroxisome proliferator‐activated receptor α

Fukui, Yuka; Motojima, Kiyoto

doi:10.1046/j.1463-1326.2002.00215.x

Cited by 47 publications

(37 citation statements)

References 11 publications

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“…Thus, severely decreased resistin mRNA levels have been observed in different mouse models of obesity and insulin resistance such as ob/ob, db/db, tub/tub, and KKA γ mice (Table 1) [60]. These findings are supported and extended by other groups indicating that resistin is down-regulated in diet-induced obesity in mice [61], in fructose-fed obese rats [62], in fa/fa rats [63], and in KK mice [64]. Paradoxically, weight loss further inhibits resistin mRNA expression in obese fa/fa rats [63].…”

Section: Resistinsupporting

confidence: 54%

“…In contrast, up-regulation of resistin mRNA expression has been observed after treatment of male ob/ob mice and ZDF rats with the PPARγ-agonists MC-555, rosiglitazone, and GW1929 for 7 days [60]. Similarly, consistent upregulation of resistin mRNA has been shown in white fat after treatment with the PPARγ-agonists NC-2100, pioglitazone, and troglitazone [64]. Various hormones regulate resistin mRNA and protein expression in vivo and in vitro; however, again results are often contradictory.…”

Section: Resistinmentioning

confidence: 95%

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Regulation of adipocytokines and insulin resistance

2003

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It has long been known that obesity and insulin resistance are linked. Recently, it has been shown that adipocytes secrete several proteins including tumour necrosis factor-α, interleukin-6, resistin, and adiponectin. Since several of these so-called adipocytokines influence insulin sensitivity and glucose metabolism profoundly, they might provide a molecular link between increased adiposity and impaired insulin sensitivity. Thiazolidinediones which decrease insulin resistance and are used in the treatment of Type 2 diabetes seem to mediate part of their insulin-sensitising effects via modulation of adipocytokine expression.Furthermore, hormones such as β-adrenergic agonists, insulin, glucocorticoids, and growth hormone might impair insulin sensitivity at least in part via up-regulation or down-regulation of adipocytokine synthesis. We summarise the current knowledge on how major adipocyte-secreted proteins are regulated by hormones and drugs influencing insulin sensitivity and discuss its implications for insulin resistance and obesity. [Diabetologia (2003[Diabetologia ( ) 46:1594[Diabetologia ( -1603

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Section: Resistinsupporting

confidence: 54%

Section: Resistinmentioning

confidence: 95%

Regulation of adipocytokines and insulin resistance

2003

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“…However, adipose tissue is also an active endocrine organ that secretes numerous circulating proteins, some with potent effects on energy and intermediary metabolism and on insulin signaling (9,(17)(18)(19). Consistent with this postulate, the insulin-sensitizing effects of peroxisome proliferator-activated receptor-γ (PPAR-γ) agonists (20) may be partly caused by the regulation of the biosynthesis and secretion of adipose-derived proteins such as resistin (9,21,22) and Acrp30/ adiponectin (23). Of interest, resistin is expressed at higher levels in intra-abdominal than subcutaneous fat depots in human (24).…”

Section: Discussionmentioning

confidence: 94%

Role of resistin in diet-induced hepatic insulin resistance

et al. 2004

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Resistin is an adipose-derived hormone postulated to link adiposity to insulin resistance. To determine whether resistin plays a causative role in the development of diet-induced insulin resistance, we lowered circulating resistin levels in mice by use of a specific antisense oligodeoxynucleotide (ASO) directed against resistin mRNA and assessed in vivo insulin action by the insulin-clamp technique. After 3 weeks on a high-fat (HF) diet, mice displayed severe insulin resistance associated with an approximately 80% increase in plasma resistin levels. In particular, the rate of endogenous glucose production (GP) increased more than twofold compared with that in mice fed a standard chow. Treatment with the resistin ASO for 1 week normalized the plasma resistin levels and completely reversed the hepatic insulin resistance. Importantly, in this group of mice, the acute infusion of purified recombinant mouse resistin, designed to acutely elevate the levels of circulating resistin up to those observed in the HF-fed mice, was sufficient to reconstitute hepatic insulin resistance. These results provide strong support for a physiological role of resistin in the development of hepatic insulin resistance in this model.

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“…Reports correlating expression levels for ADSF or circulating ADSF levels with genetic or diet-induced obesity in rodents were inconsistent (27)(28)(29). Furthermore, human studies attempting to demonstrate ADSF expression correlating with pathophysiology of obesity and type 2 diabetes (24)(25)(26) have been controversial at best.…”

Section: Discussionmentioning

confidence: 99%

Dominant inhibitory adipocyte-specific secretory factor (ADSF)/resistin enhances adipogenesis and improves insulin sensitivity

Kim

Zhao

Moon

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

109

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Adipocyte-specific secretory factor (ADSF)͞resistin is a small cysteinerich protein secreted from adipose tissue that belongs to a gene family found in inflammatory zone (FIZZ) or found in resistin-like molecule (RELM). ADSF has been implicated in modulating adipogenesis and insulin resistance. To examine the long-term function of ADSF in adipogenesis and glucose homeostasis, we constructed an expression vector for a dominant inhibitory form of ADSF by fusing it to the human IgG␥ constant region (hFc). ADSF-hFc not only homodimerizes but heterooligomerizes with ADSF͞resistin and prevents ADSF͞resis-tin inhibition of adipocyte differentiation of 3T3-L1 cells in a dominant negative manner. Transgenic mice overexpressing ADSF-hFc in adipose tissue show increased adiposity with elevated expression of adipocyte markers as well as enlarged adipocyte size. This finding clearly demonstrates in vivo the inhibitory role of ADSF in adipogenesis. ADSF-hFc transgenic mice with impaired ADSF function exhibit improved glucose tolerance and insulin sensitivity either on chow or high-fat diets. Because of the enhanced adipocyte differentiation, the ADSF-hFc transgenic mice show increased expression of leptin and adiponectin in adipose tissue. The elevated circulating levels for these adipocyte-derived hormones with decreased plasma triglyceride and free fatty acid levels may account for the improved glucose and insulin tolerance in these transgenic mice.O besity is a prevalent health hazard in industrialized countries and is closely associated with insulin resistance and type 2 diabetes. Obesity arises from increased size of adipocytes caused by lipid accumulation and from an increased number of adipocytes arising from differentiation of adipose precursor cells to mature adipocytes under the appropriate nutritional and hormonal conditions (1). Gene expression studies during adipocyte differentiation have firmly established that peroxisome proliferator-activated receptor ␥ (PPAR␥) and the CCAAT enhancer-binding protein (C͞EBP) family of transcription factors play central roles in adipocyte differentiation (2, 3). However, various factors in cell-cell and cell-matrix communications govern expression of the adipocyte transcription factors and therefore regulate conversion of preadipocytes to adipocytes (4). Although adipose tissue serves as the major energy reservoir in higher eukaryotes, the role of adipose tissue as a secretory organ has emerged through the discovery of leptin (5). In addition to leptin, other secretory factors including adiponectin and tumor necrosis factor ␣, as well as preadipocytespecific preadipocyte factor 1 (Pref-1) are known to be secreted from adipose tissue (6-8). These factors are involved in regulating a variety of physiological functions including satiety and energy metabolism, as well as adipocyte differentiation. In this regard, we have shown that Pref-1, which is secreted specifically by preadipocytes, inhibits adipocyte differentiation (8-10).We previously identified adipocyte-specific secretory ...

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Expression of resistin in the adipose tissue is modulatedby various factors including peroxisome proliferator‐activated receptor α

Abstract: Our results indicated that diverse factors modulate the expression of resistin in the adipose tissues of mice, and suggested that resistin is not a master hormone linking obesity to diabetes.

Cited by 47 publications

References 11 publications

Regulation of adipocytokines and insulin resistance

Regulation of adipocytokines and insulin resistance

Role of resistin in diet-induced hepatic insulin resistance

Dominant inhibitory adipocyte-specific secretory factor (ADSF)/resistin enhances adipogenesis and improves insulin sensitivity

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