Resistin messenger-RNA expression is increased by proinflammatory cytokines in vitro

Kaser, Susanne; Kaser, Arthur; Sandhofer, A.; Ebenbichler, Christoph; Tilg, Herbert; Patsch, Josef R.

doi:10.1016/j.bbrc.2003.07.003

Cited by 431 publications

(368 citation statements)

References 33 publications

Supporting

Mentioning

339

Contrasting

Unclassified

Order By: Relevance

“…The biological role of resistin in humans is still controversial [49] and seems to differ for several aspects from what described in rodents. Indeed, in rodents resistin is up-regulated in dietinduced or genetic obesity [70] whereas in humans seems to have a role in sustaining inflammation, as shown by studies in which resistin is up-regulated in monocytes exposed to proinflammatory stimuli and in conditions of experimentally induced endotoxemia [71,72]. In relation to liver fibrogenesis, it has been shown that resistin expression during liver injury positively correlates with infiltration of inflammatory cells, which may represent the principal source of intrahepatic resistin [73].…”

Section: Adipokinesmentioning

confidence: 99%

Cellular and molecular mechanisms in liver fibrogenesis

Novo

Cannito

Paternostro

et al. 2014

Archives of Biochemistry and Biophysics

179

194

View full text Add to dashboard Cite

Section: Adipokinesmentioning

confidence: 99%

Cellular and molecular mechanisms in liver fibrogenesis

Novo

Cannito

Paternostro

et al. 2014

Archives of Biochemistry and Biophysics

179

194

View full text Add to dashboard Cite

“…67 While in rodents resistin is predominantly expressed in adipocytes, peripheral blood mononuclear cells seem to be a major source of resistin in humans. 68 At the protein level, mouse and human resistin show remarkable similarities with respect to the conserved cysteine residues that are reportedly involved in the dimerization process. 69 Interestingly, resistin mRNA and protein expression were also detected in human pancreatic islets.…”

Section: Resistinmentioning

confidence: 99%

Role of glucocorticoids in the physiopathology of excessive fat deposition and insulin resistance

2004

View full text Add to dashboard Cite

Glucocorticoids are important hormones in the regulation of metabolic homeostasis. We infused normal rats with dexamethasone given intracerebroventricularly (i.c.v.) for 3 days. This resulted in hyperphagia, hyperinsulinemia, and marked insulin resistance. Similar metabolic defects were observed following i.c.v. infusion of neuropeptide Y (NPY) in normal rats. As central dexamethasone infusion enhanced NPY content in the arcuate nucleus, it suggested that its metabolic effects are mediated by NPY. Moreover, due to the lack of effects observed in vagotomized animals, activation of the parasympathetic nervous system by central dexamethasone infusion is proposed. Glucocorticoid action is known to involve prereceptor metabolism by enzymes such as 11b-HSD-1 that converts inactive into active glucocorticoids. Mice overexpressing 11b-HSD-1 in adipose tissue were shown to be obese and insulin resistant. We recently observed that adipose tissue 11b-HSD-1 mRNA expression is increased at the onset of high-fat diet-induced obesity and positively correlated with the degree of hyperglycemia. In human obesity, increased adipose tissue 11b-HSD-1 expression and activity were also reported. Resistin is a new adipose tissue-secreted hormone shown to play a role in glucose homeostasis by increasing hepatic glucose production and inhibiting muscle and adipose tissue glucose utilization. We observed increased adipose tissue resistin expression in the early phase of highfat diet-induced obesity as well as decreased resistin expression in response to leptin. A positive correlation between glycemia and adipose tissue resistin expression further suggested a role of this hormone in the development of insulin resistance. The melanocortin system is another important player in the regulation of energy balance. Peripheral administration of a melanocortin agonist decreased food intake and body weight and favored lipid oxidation, effects that were more marked in obese than in lean rats. It is proposed that both resistin and melanocortin agonists may influence adipose tissue 11b-HSD-1, thereby decreasing or enhancing glucose metabolism.

show abstract

“…It has been demonstrated that proinflammatory mediators such as TNF-α, IL-1β, IL-6, or lipopolysaccharide (LPS) can strongly increase the expression of resistin in peripheral blood mononuclear cells (PBMCs), suggesting a role for resistin in the process of inflammation [36][37][38][39]. In addition, C-reactive protein (CRP) induced both mRNA expression and protein secretion of resistin in a dose-and time-dependent manner in PBMCs [40].…”

mentioning

confidence: 99%