Regulation of Leptin by Steroid Hormones in Rat Adipose Tissue

Kristensen, Kurt; Pedersen, Steen B.; Richelsen, Bjørn

doi:10.1006/bbrc.1999.0842

Cited by 93 publications

(64 citation statements)

References 24 publications

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“…Leptin is the main regulator of feeding behaviour (Szanto & Kahn 2000). It has been reported that loss of ovarian function determines an increase in food intake (Wade 1975), and that ovariectomy-induced weight gain is caused by a decrease in leptin concentration (Chu et al 1999), which could be prevented by 17 -oestradiol treatment (Kristensen et al 1999). In this context, it has been proposed that leptin and insulin signalling networks may be connected at the level of IRS-1 (Szanto & Kahn 2000), but most evidence seems to suggest that there is a tissue-specific interaction between leptin and insulin that is quite variable.…”

Section: Discussionmentioning

confidence: 99%

Dose- and time-dependent effects of 17beta-oestradiol on insulin sensitivity in insulin-dependent tissues of rat: implications of IRS-1

González

Alonso²,

Dı́az³

et al. 2003

Journal of Endocrinology

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Numerous studies have suggested that ovarian hormones are able to modulate insulin sensitivity, but their exact role remains unclear. We have investigated whether different doses of 17 -oestradiol mediate changes in insulin sensitivity and if these changes could be related to modifications of insulin receptor substrate-1 (IRS-1). Female rats were ovariectomized and later separated into three groups: untreated; treated with a dose of 17 -oestradiol sufficient to reproduce gestational plasma concentrations of 17 -oestradiol (group E); and treated with a dose 100 times greater than that given to group E (group E2). A euglycaemic-hyperinsulinaemic clamp was used to measure insulin sensitivity. Changes in IRS-1 were analysed by Western blotting and RT-PCR assays. In group E we found a decrease in insulin sensitivity between days 11 and 16 of treatment as in late gestation, whereas in the untreated group and group E2, development of insulin resistance was observed throughout the treatment. In contrast, whereas in group E2 insulin resistance throughout the hormonal treatment was related to diminished expression and phosphorylation of IRS-1, in group E the decrease in insulin sensitivity between days 11 and 16 of treatment was not related to a decrease in IRS-1 expression. Our results suggest that the effects of oestradiol on insulin sensitivity were dose-dependent and that the insulin resistance associated with a high dose of 17 -oestradiol was related to downregulation of IRS-1 expression.

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Section: Discussionmentioning

confidence: 99%

Dose- and time-dependent effects of 17beta-oestradiol on insulin sensitivity in insulin-dependent tissues of rat: implications of IRS-1

González

Alonso²,

Dı́az³

et al. 2003

Journal of Endocrinology

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“…After puberty, estrogen and testosterone modulate leptin synthesis and secretion from adipocytes, via sex steroid-dependent transcriptional mechanisms (Machinal et al 1999, Haifei et al 2009). Moreover, exposure of human adipose cells to testosterone or 5a-dihydrotestosterone (DHT), inhibits leptin expression (Wabitsch et al 1997), whereas 17b-estradiol (E 2 ) treatment increases adipose tissue leptin mRNA levels in female rats (Kristensen et al 1999).…”

Section: Brown Adipose Tissue and Obesitymentioning

confidence: 99%

Role of sex hormones in modulation of brown adipose tissue activity

Quarta

Mazza²,

Pasquali³

et al. 2012

Journal of Molecular Endocrinology

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The recent demonstration that metabolically active brown adipose tissue (BAT) is present with a high prevalence in humans undoubtedly represents one of the major advancements in the field of metabolic research in the last few years. The increasing interest in BAT is justified by preclinical observations highlighting an important role of this tissue in energy dissipation and metabolic clearance of substrates from the blood. These findings imply that stimulation of BAT activity may represent a new therapeutic approach for obesity and associated comorbidities. However, before proposing BAT as a target organ for therapeutics in a clinical setting, many further notions about BAT function and modulation need to be explored. Keeping in mind the importance of sex dimorphism in energy metabolism control under physiological and pathological conditions, sex hormones may play a relevant role in the regulation of BAT activity in both males and females. Much of the evidence acquired in the past supports the concept of an important role for different sex hormones in BAT thermogenesis and indicates that this tissue mediates the ability of sex hormones to modulate energy balance. These findings make it plausible that a modified interaction between BAT and sex hormones may contribute to the development and the maintenance of obesity and associated metabolic complications.Journal of Molecular Endocrinology (2012) 49, R1-R7

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“…All subsequent procedures were carried out under a laminar airflow hood and under sterile conditions. The tissue was placed in Medium 199, minced into fragments of less than 10 mg each, rinsed in NaCl and incubated as previously described (Kristensen et al, 1999). In brief, 500 mg of adipose tissue fragments were placed in 50 ml plastic tubes containing 5 ml serum-free Medium 199 without phenol red, supplemented with 25 mM HEPES, 1% bovine serum albumin, 1 nM insulin, antipain and leupeptin 20 µl/100 ml and penicillin and streptomycin (10 000 IU) 1 ml/100 ml.…”

Section: Introductionmentioning

confidence: 99%