Leptin's Role in Lipodystrophic and Nonlipodystrophic Insulin-Resistant and Diabetic Individuals

Author:

Moon Hyun-Seuk1,Dalamaga Maria2,Kim Sang-Yong13,Polyzos Stergios A.4,Hamnvik Ole-Petter15,Magkos Faidon1,Paruthi Jason1,Mantzoros Christos S.16

Affiliation:

1. Division of Endocrinology, Diabetes, and Metabolism (H.-S.M., S.-Y.K., O.-P.H., F.M., J.P., C.S.M.), Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215;

2. Department of Clinical Biochemistry (M.D.), Attikon General University Hospital, Athens University Medical School, Athens 15784, Greece;

3. Division of Endocrinology and Metabolism (S.-Y.K.), School of Medicine, Chosun University, Gwang-Ju 501-717, South Korea;

4. Second Medical Clinic (S.A.P.), Aristotle University of Thessaloniki, Ippokration Hospital, Thessaloniki 11527, Greece;

5. Division of Endocrinology, Diabetes, and Hypertension (O.-P.H.), Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115;

6. Section of Endocrinology (C.S.M.), Boston VA Healthcare System, Harvard Medical School, Boston, Massachusetts 02118

Abstract

Abstract Leptin is an adipocyte-secreted hormone that has been proposed to regulate energy homeostasis as well as metabolic, reproductive, neuroendocrine, and immune functions. In the context of open-label uncontrolled studies, leptin administration has demonstrated insulin-sensitizing effects in patients with congenital lipodystrophy associated with relative leptin deficiency. Leptin administration has also been shown to decrease central fat mass and improve insulin sensitivity and fasting insulin and glucose levels in HIV-infected patients with highly active antiretroviral therapy (HAART)-induced lipodystrophy, insulin resistance, and leptin deficiency. On the contrary, the effects of leptin treatment in leptin-replete or hyperleptinemic obese individuals with glucose intolerance and diabetes mellitus have been minimal or null, presumably due to leptin tolerance or resistance that impairs leptin action. Similarly, experimental evidence suggests a null or a possibly adverse role of leptin treatment in nonlipodystrophic patients with nonalcoholic fatty liver disease. In this review, we present a description of leptin biology and signaling; we summarize leptin's contribution to glucose metabolism in animals and humans in vitro, ex vivo, and in vivo; and we provide insights into the emerging clinical applications and therapeutic uses of leptin in humans with lipodystrophy and/or diabetes.

Publisher

The Endocrine Society

Subject

Endocrinology,Endocrinology, Diabetes and Metabolism

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