Metformin treatment does not affect total leptin levels and free leptin index in obese patients with polycystic ovary syndrome

Romualdi, Daniela; Campagna, Giuseppe; Selvaggi, Luigi; Cento, R. M.; Proto, Caterina; Lanzone, Antonio; Guido, Maurizio

doi:10.1016/j.fertnstert.2007.05.004

Cited by 22 publications

(20 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As has been reported previously, 4 months therapy with metformin (1500 mg daily) in seven obese women with hyperinsulinemia and PCOS did not affect the sOBR levels (Romualdi et al 2008). It is possible that in the presence of high circulating levels of other hormones, metformin-stimulated signaling pathways are blunted and other regulatory mechanisms become more prominent.…”

Section: Discussionsupporting

confidence: 59%

Metformin increases hepatic leptin receptor and decreases steatosis in mice

Tang

Xiang

et al. 2016

Journal of Endocrinology

View full text Add to dashboard Cite

In addition to the ascertained efficacy as antidiabetic drug, metformin is increasingly being used as weight-loss agent in obesity, and as insulin sensitizer in nonalcoholic fatty liver disease (NAFLD). However, the mechanisms underlying these effects are still incompletely understood. Emerging evidence suggest metformin as leptin sensitizer to mediate the weight-loss effect in the brain. In this study, we investigated effects of metformin on expression of leptin receptors in liver and kidney in mice. C57BL/6 mice were fed with chow diet (CD) or high-fat diet (HF) for 5 months. Afterward, mice were treated with metformin (50 mg/kg or 200 mg/kg) for 15 days. Metabolic parameters and hepatic gene expression were analyzed at the end of the treatment. We also tested the effects of metformin on plasma-soluble leptin receptor (sOB-R) levels in newly diagnosed type 2 diabetes mellitus (T2DM) patients, and assessed its effect on hepatosteatosis in mice. Results showed that metformin upregulates the expression of leptin receptors (OB-Ra, -Rb, -Rc, and -Rd) in liver but not kidney. The stimulation effect is dosedependent in both chow and HF mice. Upregulation of OB-Rb, long signaling isoform, needs a relatively higher dose of metformin. This effect was paralleled by increased sOBR levels in mice and T2DM patients, and decreased hepatic triglyceride (TG) content and lipogenic gene expression, including sterol regulatory element-binding protein 1c (SREBP-1c), fatty acid synthase (FAS) and acetyl-CoA carboxylase-1 (ACC-1). Taken together, these data identify hepatic leptin receptor as target gene being upregulated by metformin which may enhance leptin sensitivity in liver to alleviate steatosis.

show abstract

Section: Discussionsupporting

confidence: 59%

Metformin increases hepatic leptin receptor and decreases steatosis in mice

Tang

Xiang

et al. 2016

Journal of Endocrinology

View full text Add to dashboard Cite

show abstract

“…Moreover, after controlling for BMI, no significant correlation was found between serum leptin levels and HOMA or hyperinsulinemia after glucose challenge in either obese or normal weight women with PCOS (431). Furthermore, neither troglitazone nor metformin, which increase insulin sensitivity, affected serum leptin concentrations (432,433).…”

Section: Pcos and Adipokinesmentioning

confidence: 87%

Adipose tissue and reproduction in women

Bohler

Mokshagundam

Winters

2010

Fertility and Sterility

View full text Add to dashboard Cite

“…As with BMI reduction, the effect of metformin on central adiposity appears to be maximized at higher doses, up to 2500 mg/day (132). Nevertheless, metformin treatment does not appear to significantly alter adipokine secretion in women with PCOS (140,141).…”

Section: Disorders Of Glucose Tolerancementioning

confidence: 88%

“…In a meta-analysis of RCTs conducted in these patients, metformin therapy resulted in significant decreases in systolic blood pressure (SBP) and in low density lipoprotein (LDL)-cholesterol levels (74). Subsequent RCTs in overweight and obese patients have also shown that metformin treatment, without any specific lifestyle modification, lowers SBP (142) and promotes a less atherogenic lipid profile (12,133,141). Some investigators have reported lower total cholesterol and LDL-cholesterol levels (12,133), while others have shown higher high density lipoprotein (HDL) levels following a 3-6-month treatment (141).…”

Section: Other Cardiovascular Risk Factors and Markersmentioning

confidence: 99%

Metformin: an old medication of new fashion: evolving new molecular mechanisms and clinical implications in polycystic ovary syndrome

Diamanti-Kandarakis

Christakou

Kandaraki

et al. 2010

European Journal of Endocrinology

208

184

View full text Add to dashboard Cite

Polycystic ovary syndrome (PCOS) is now recognized to be the most common endocrinopathy in women of reproductive age with a prevalence of 6.6-6.8%. PCOS, a syndrome of unknown etiology, was initially regarded as a reproductive disorder. However, in the last 15 years the role of insulin resistance (IR) has been identified as a significant contributor to the pathogenesis of PCOS, and the metabolic and cardiovascular sequelae of the syndrome have been increasingly appreciated. The coexistence and interaction of reproductive and cardiometabolic abnormalities in the context of PCOS have created a need for a modified therapeutic management of affected women. Insulin sensitizers, particularly metformin, have been introduced as a pharmaceutical option targeting not only IR, but several other aspects of the syndrome, including reproductive abnormalities. The landscape of the multifaceted actions of metformin evolves to broaden the therapeutic implications of this old drug in a new fashion for patients with PCOS. Most recently, the spectrum of metformin's targets has been expanded, and molecular studies have explored the tissue-specific mechanisms of metformin in the liver, the muscle, the endothelium, and the ovary. The use of metformin in pregnant women with PCOS comprises another scarcely explored, but promising area of research. This review attempts to cover the spectrum of metformin's cellular actions in different tissues and to summarize the current literature regarding the potential medical value of this medication in PCOS. Even if many of these actions are individually modest, they seem to be collectively sufficient to confer therapeutic benefits not only in cardiometabolic aspects but also in reproductive aspects of PCOS.

show abstract

Metformin treatment does not affect total leptin levels and free leptin index in obese patients with polycystic ovary syndrome

Cited by 22 publications

References 22 publications

Metformin increases hepatic leptin receptor and decreases steatosis in mice

Metformin increases hepatic leptin receptor and decreases steatosis in mice

Adipose tissue and reproduction in women

Metformin: an old medication of new fashion: evolving new molecular mechanisms and clinical implications in polycystic ovary syndrome

Contact Info

Product

Resources

About