Leptin Production by Encapsulated Adipocytes Increases Brown Fat, Decreases Resistin, and Improves Glucose Intolerance in Obese Mice
| Autor: | Ouliana Ziouzenkova, Emiliano Melgar-Bermudez, Chen Gilor, David DiSilvestro, Anuradha Kalyanasundaram, L. James Lee, Rumana Yasmeen, Paolo Fadda |
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| Přispěvatelé: | Aguila, Marcia B |
| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Leptin Male Physiology Peptide Hormones medicine.medical_treatment Messenger Mice Obese lcsh:Medicine Adipose tissue Biochemistry Obese Oral and gastrointestinal Fats chemistry.chemical_compound Mice Endocrinology 0302 clinical medicine Adipose Tissue Brown Animal Cells Adipocyte Brown adipose tissue Medicine and Health Sciences Adipocytes Insulin 2.1 Biological and endogenous factors Resistin Aetiology lcsh:Science Cells Cultured Connective Tissue Cells Glucose Tolerance Multidisciplinary Cultured Blotting Reverse Transcriptase Polymerase Chain Reaction Diabetes Cell Differentiation Lipids 3. Good health Stroke medicine.anatomical_structure Physiological Parameters Adipose Tissue Connective Tissue Brown Adipose Tissue Cellular Types Anatomy medicine.symptom Western hormones hormone substitutes and hormone antagonists Research Article medicine.medical_specialty General Science & Technology Cells Blotting Western Inflammation Biology Real-Time Polymerase Chain Reaction 03 medical and health sciences Insulin resistance Internal medicine 3T3-L1 Cells Glucose Intolerance medicine Animals RNA Messenger Obesity Metabolic and endocrine Nutrition Diabetic Endocrinology Body Weight lcsh:R Biology and Life Sciences Brown Cell Biology medicine.disease Hormones Biological Tissue Metabolism 030104 developmental biology chemistry RNA lcsh:Q Insulin Resistance 030217 neurology & neurosurgery |
| Zdroj: | PloS one, vol 11, iss 4 PLoS ONE, Vol 11, Iss 4, p e0153198 (2016) PLoS ONE |
| Popis: | The neuroendocrine effects of leptin on metabolism hold promise to be translated into a complementary therapy to traditional insulin therapy for diabetes and obesity. However, injections of leptin can provoke inflammation. We tested the effects of leptin, produced in the physiological adipocyte location, on metabolism in mouse models of genetic and dietary obesity. We generated 3T3-L1 adipocytes constitutively secreting leptin and encapsulated them in a poly-L-lysine membrane, which protects the cells from immune rejection. Ob/ob mice (OB) were injected with capsules containing no cells (empty, OB[Emp]), adipocytes (OB[3T3]), or adipocytes overexpressing leptin (OB[Lep]) into both visceral fat depots. Leptin was found in the plasma of OB[Lep], but not OB[Emp] and OB[3T3] mice at the end of treatment (72 days). The OB[Lep] and OB[3T3] mice have transiently suppressed appetite and weight loss compared to OB[Emp]. Only OB[Lep] mice have greater brown fat mass, metabolic rate, and reduced resistin plasma levels compared to OB[Emp]. Glucose tolerance was markedly better in OB[Lep] vs. OB[Emp] and OB[3T3] mice as well as in wild type mice with high-fat diet-induced obesity and insulin resistance treated with encapsulated leptin-producing adipocytes. Our proof-of-principle study provides evidence of long-term improvement of glucose tolerance with encapsulated adipocytes producing leptin. |
| Databáze: | OpenAIRE |
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