Central administration of resistin promotes short-term satiety in rats

Tovar, Sulay; Nogueiras, Rubén; Tung, L. Y. C.; Castañeda, Tamara R.; Vázquez, María J.; Morris, Amanda J.; Williams, Lynda M.; Dickson, Suzanne L.; Diéguez, Carlos

doi:10.1530/eje.1.01999

Cited by 89 publications

(64 citation statements)

References 17 publications

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“…ERK1/2-MAPK phosphorylation was only affected in rat GCs. Protein and mRNA expression of resistin have been described in several tissues of the reproductive axis (Morash et al 2002, Nogueiras et al 2004, Brown et al 2005, Tovar et al 2005. Furthermore, resistin mRNA is expressed in the bovine mammary gland, and its expression in this tissue decreases during lactation (Komatsu et al 2003).…”

Section: Discussionmentioning

confidence: 99%

“…Indeed, expression of resistin (mRNA and protein) has been reported in several reproductive tissues including hypothalamus (Morash et al 2002, Tovar et al 2005, pituitary (Morash et al 2002, Brown et al 2005, and testis (Nogueiras et al 2004). In hypothalamus, resistin has been shown to inhibit feeding (Tovar et al 2005, Vazquez et al 2008.…”

Section: Introductionmentioning

confidence: 99%

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Expression and effect of resistin on bovine and rat granulosa cell steroidogenesis and proliferation

Maillard¹,

Froment²,

Ramé³

et al. 2011

Reproduction

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Resistin, initially identified in adipose tissue and macrophages, was implicated in insulin resistance. Recently, its mRNA was found in hypothalamo-pituitary axis and rat testis, leading us to hypothesize that resistin may be expressed in ovary. In this study, we determined in rats and cows 1) the characterization of resistin in ovary by RT-PCR, immunoblotting, and immunohistochemistry and 2) the effects of recombinant resistin (10, 100, 333, and 667 ng/ml)GIGF1 (76 ng/ml) on steroidogenesis, proliferation, and signaling pathways of granulosa cells (GC) measured by enzyme immunoassay, [3 H]thymidine incorporation, and immunoblotting respectively. We observed that resistin mRNA and protein were present in several bovine and rat ovarian cells. Nevertheless, only bovine GC abundantly expressed resistin mRNA and protein. Resistin treatment decreased basal but not IGF1-induced progesterone (P!0.05; whatever the dose) and estradiol (P!0.005; for 10 and 333 ng/ml) production by bovine GC. In rats, resistin (10 ng/ml) increased basal and IGF1-induced progesterone secretion (P!0.0001), without effect on estradiol release. We found no effect of resistin on rat GC proliferation. Conversely, in cows, resistin increased basal proliferation (P!0.0001; for 100-667 ng/ml) and decreased IGF1-induced proliferation of GC (P!0.0001; for 10-333 ng/ml) associated with a decrease in cyclin D2 protein level (P!0.0001). Finally, resistin stimulated AKT and p38-MAPK phosphorylation in both species, ERK1/2-MAPK phosphorylation in rats and had the opposite effect on the AMPK pathway (P!0.05). In conclusion, our results show that resistin is expressed in rat and bovine ovaries. Furthermore, it can modulate GC functions in basal state or in response to IGF1 in vitro.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Expression and effect of resistin on bovine and rat granulosa cell steroidogenesis and proliferation

Maillard¹,

Froment²,

Ramé³

et al. 2011

Reproduction

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“…The resistin levels, however, were significantly higher in the HO group, suggesting that they may be raised due to mechanisms other than insulin resistance. The hypothalamic action of resistin is unclear, but animal studies have demonstrated that central administration of resistin reduces food intake in the short term (52,53). Resistin receptors are present within the hypothalamus, in particular the arcuate and ventromedial nuclei (53,52).…”

Section: Adiponectin and Resistinmentioning

confidence: 99%

Hyperleptinaemia rather than fasting hyperinsulinaemia is associated with obesity following hypothalamic damage in children

Shaikh¹,

Grundy

Kirk³

2008

European Journal of Endocrinology

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Background: Obesity following hypothalamic damage is often severe and resistant to lifestyle changes. Disruption of hypothalamic feedback mechanisms that maintain energy homeostasis may be responsible for this intractable obesity. Adipocytokines including insulin and leptin are also known to be important regulators of appetite and weight. Objective: To investigate the role of insulin, leptin, adiponectin and resistin in the aetiology of hypothalamic obesity (HO). Design: This was a cross-sectional study of three groups of children, those with HO, congenital hypopituitarism (CH) and simple obesity (SO). Results: A total of 69 children (HOZ28, CHZ18, SOZ23) had leptin, resistin, adiponectin and insulin measured. Although fasting hyperinsulinaemia and insulin resistance were demonstrated, no differences in insulin or insulin resistance were seen between the groups. The HO group, however, had higher levels of leptin, adiponectin and resistin, which persisted even after adjusting for fat mass, compared with the other groups (P!0.05). Conclusion: No differences in fasting hyperinsulinaemia or insulin resistance were seen between the groups; however, leptin levels are elevated, even after adjusting for fat mass, suggesting that an element of leptin resistance is associated with HO. This is consistent with the inability of leptin to act on the hypothalamus, either due to transport across the blood-brain barrier or dysfunctional receptors. The lack of response to leptin may be more important in the development of obesity in these individuals, and the fasting hyperinsulinaemia is a result of the increased adipose tissue rather than the cause of the weight gain.

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“…We have found that loss of resistin in leptin-deficient mice exacerbates obesity by further decreasing energy expenditure, but insulin sensitivity is enhanced (R.S.A., unpublished data). Recent reports have described inhibition of food intake and induction of hepatic insulin resistance by intracerebroventricular resistin administration (90,91).…”

Section: Role Of Leptin In Famine and Feastmentioning

confidence: 99%

Brain Adipocytokine Action and Metabolic Regulation

et al. 2006

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Adipose tissue secretes factors that control various physiological systems. The fall in leptin during fasting mediates hyperphagia and suppresses thermogenesis, thyroid and reproductive hormones, and immune system. On the other hand, rising leptin levels in the fed state stimulate fatty acid oxidation, decrease appetite, and limit weight gain. These divergent effects of leptin occur through neuronal circuits in the hypothalamus and other brain areas. Leptin also regulates the activities of enzymes involved in lipid metabolism, e.g., AMP-activated protein kinase and stearoyl-CoA desaturase-1, and also interacts with insulin signaling in the brain. Adiponectin enhances fatty acid oxidation and insulin sensitivity, in part by stimulating AMP-activated protein kinase phosphorylation and activity in liver and muscle. Moreover, adiponectin decreases body fat by increasing energy expenditure and lipid catabolism. These effects involve peripheral and possibly central mechanisms. Adipose tissue mediates interconversion of steroid hormones and secretes proinflammatory cytokines, vasoactive peptides, and coagulation and complement proteins. Understanding the actions of these "adipocytokines" will provide insight into the pathogenesis and treatment of obesity and related diseases. Diabetes 55 (Suppl. 2): S145-S154, 2006 ADIPOSE TISSUE

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Central administration of resistin promotes short-term satiety in rats

Cited by 89 publications

References 17 publications

Expression and effect of resistin on bovine and rat granulosa cell steroidogenesis and proliferation

Expression and effect of resistin on bovine and rat granulosa cell steroidogenesis and proliferation

Hyperleptinaemia rather than fasting hyperinsulinaemia is associated with obesity following hypothalamic damage in children

Brain Adipocytokine Action and Metabolic Regulation

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