Estradiol Supplementation Helps Overcome Central Leptin Resistance of Ovariectomized Mice on a High Fat Diet

Matyšková, Resha; Železná, Blanka; Maixnerová, Jana; Koutová, D.; Haluzı́k, Martin; Maletı́nská, Lenka

doi:10.1055/s-0029-1243250

Cited by 31 publications

(24 citation statements)

References 24 publications

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“…The estrogen effects were found to be independent of leptin, and they were able to substitute for leptin anorexigenic effects in leptin-or leptin-receptor deficient mice (Gao et al, 2007). Similarly in our study, in marked diet-induced obesity, which is also considered to be a leptin-resistant state (Matyšková et al, 2010), four weeks of estrogen supplementation significantly decreased the body weight of OVX mice fed on HF diet and normalized metabolic parameters.…”

Section: Discussionsupporting

confidence: 82%

“…In a previous study by our group, OVX mice fed HF diet were extremely prone to diet-induced obesity (DIO), which resulted in hyperleptinemia, hyperinsulinemia, hyperglycemia, and resistance to centrally administered leptin. Estrogen supplementation normalized central resistance to exogenous leptin and reduced the fat/body weight ratio and leptin and glucose levels (Matyšková et al, 2010).…”

Section: Introductionmentioning

confidence: 98%

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The Peptidic GHS-R antagonist [D-Lys3]GHRP-6 markedly improves adiposity and related metabolic abnormalities in a mouse model of postmenopausal obesity

Maletı́nská

Matyšková

Maixnerová

et al. 2011

Molecular and Cellular Endocrinology

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Section: Discussionsupporting

confidence: 82%

Section: Introductionmentioning

confidence: 98%

The Peptidic GHS-R antagonist [D-Lys3]GHRP-6 markedly improves adiposity and related metabolic abnormalities in a mouse model of postmenopausal obesity

Maletı́nská

Matyšková

Maixnerová

et al. 2011

Molecular and Cellular Endocrinology

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“…It has been reported that OVX mice do not respond to injected leptin, whereas estradial-supplemented mice show a significant reduction in body weight [23]. Our results show moderate leptin resistance in OVX-control mice compared to sham mice.…”

Section: Discussionsupporting

confidence: 45%

Androgen (dihydrotestosterone)–mediated regulation of food intake and obesity in female mice

Kanaya

Vonderfecht

Chen

2013

The Journal of Steroid Biochemistry and Molecular Biology

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To better understand how elevated androgen levels regulate food intake and obesity in females, we treated ovariectomized female mice with dihydrotestosterone (non-aromatazable androgen), measured food intake and body weight, and evaluated physiological changes in liver function, glucose tolerance, and leptin resistance. Ovariectomized mice were treated with DHT or placebo. Mice were then fed a high fat diet under free-feeding or pair-feeding conditions for 3 months. We found that when DHT-treated ovariectomized mice had free access to food (free-feeding), they had increased food intake and higher body weight compared with control animals. These mice also had a significantly greater accumulation of fat in the liver and exhibited increased fasting glucose, impaired glucose tolerance, and resistance to leptin. However, when these mice were placed on a restricted diet and fed the same caloric amounts as controls (pair-feeding), their body weight increased at the same rate as control animals. This suggests that androgen regulates food intake through altered leptin sensitivity, and this increase of food intake could significantly contribute to an obesity phonotype. In summary, we demonstrated a role for androgen in the regulation of food intake and weight gain in females using a mouse model. This model will be useful to further elucidate the roles of elevated androgen in females.

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“…It has been reported that decreasing E 2 causes not only an overproduction of NPY, but also an impaired leptin sensitivity in ovariectomized rats (31). Estrogen replacement has been studied as a method to prevent increases in body weight in experimental and clinical trials (32,33). However, in the present study, the OVX+LA group exhibited less FM and FFM compared with that in the OVX group.…”

Section: Discussioncontrasting

confidence: 58%

Changes in body composition and mRNA expression of ghrelin and lipoprotein lipase in rats treated with leuprolide acetate, a GnRH agonist

et al. 2017

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Abstract. Leuprolide acetate (LA), a gonadotropin-releasing hormone (GnRH) agonist, was identified to cause changes in body weight in experimental and clinical trials; however, to date, the effect of LA on the body composition has not been properly assessed. The aim of the present study was to evaluate the long-term effect of LA administration on body composition and the mRNA expression of ghrelin and lipoprotein lipase (LPL) in rats. Ovariectomized (OVX), ovariectomized and LA-treated (OVX+LA), non-ovariectomized (CTRL) and non-ovariectomized but LA-treated (LA) rats were used. LA treatment was performed by intramuscular injection at 5 µg/kg every 72 h over 120 days. Analysis of body composition and mRNA expression of ghrelin and lipoprotein lipase were performed. The results indicated significant changes in body composition after treatment; in the OVX, LA, OVX+LA and CTRL group, the body weight was increased by 216.1, 183.7, 175.4 and 150.1%, respectively, compared with baseline. The fat mass in the LA group was 14% higher than that in the CTRL group, while that in the OVX group was 19% higher than that in the OVX+LA, and the fat-free mass was similar between the LA and CTRL as well as the OVX and OVX+LA groups. Following 120 days of treatment, the mRNA expression of ghrelin and LPL in the LA group was ~20% higher than that in the CTRL group, while that in the OVX+LA was downregulated in comparison with that in the OVX group. The results of the present study confirmed changes in body composition and mRNA expression of ghrelin and LPL caused by long-term administration of LA. LA may contribute to regulate food consumption and exert control over adipogenesis.

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Estradiol Supplementation Helps Overcome Central Leptin Resistance of Ovariectomized Mice on a High Fat Diet

Abstract: In Table 1 of the original article the values for triglycerides (mg/dl) are incorrect. The correct values are: 58.2, 66.1, 70.7 and 68.8 mg/dl.

Cited by 31 publications

References 24 publications

The Peptidic GHS-R antagonist [D-Lys3]GHRP-6 markedly improves adiposity and related metabolic abnormalities in a mouse model of postmenopausal obesity

The Peptidic GHS-R antagonist [D-Lys3]GHRP-6 markedly improves adiposity and related metabolic abnormalities in a mouse model of postmenopausal obesity

Androgen (dihydrotestosterone)–mediated regulation of food intake and obesity in female mice

Changes in body composition and mRNA expression of ghrelin and lipoprotein lipase in rats treated with leuprolide acetate, a GnRH agonist

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