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Metabolism. 2019 Aug;97:9-17. doi: 10.1016/j.metabol.2019.05.005. Epub 2019 May 18.

Pancreatic adipocytes mediate hypersecretion of insulin in diabetes-susceptible mice.

Author information

1
Department of Experimental Diabetology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), 14558 Nuthetal, Germany; German Center for Diabetes Research (DZD), München-Neuherberg 85764, Germany.
2
Department of Adipocyte Development and Nutrition, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), 14558 Nuthetal, Germany. Electronic address: Nicole.Dittberner@dife.de.
3
Department of Experimental Diabetology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), 14558 Nuthetal, Germany; German Center for Diabetes Research (DZD), München-Neuherberg 85764, Germany. Electronic address: stadion@dife.de.
4
German Center for Diabetes Research (DZD), München-Neuherberg 85764, Germany; Institute for Diabetes Research and Metabolic Diseases, Helmholtz Center Munich, Eberhard Karls University of Tübingen, 72076, Tübingen, Germany. Electronic address: Felicia.Gerst@med.uni-tuebingen.de.
5
Department of Experimental Diabetology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), 14558 Nuthetal, Germany; German Center for Diabetes Research (DZD), München-Neuherberg 85764, Germany. Electronic address: Anett.Helms@dife.de.
6
German Center for Diabetes Research (DZD), München-Neuherberg 85764, Germany; Institute for Diabetes Research and Metabolic Diseases, Helmholtz Center Munich, Eberhard Karls University of Tübingen, 72076, Tübingen, Germany; Institute of Nutritional Science, University of Potsdam, 14558 Nuthetal, Germany. Electronic address: Tim.Schulz@dife.de.
7
Department of Experimental Diabetology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), 14558 Nuthetal, Germany; German Center for Diabetes Research (DZD), München-Neuherberg 85764, Germany; Institute of Nutritional Science, University of Potsdam, 14558 Nuthetal, Germany. Electronic address: schuermann@dife.de.

Abstract

OBJECTIVE:

Ectopic fat accumulation in the pancreas in response to obesity and its implication on the onset of type 2 diabetes remain poorly understood. Intermittent fasting (IF) is known to improve glucose homeostasis and insulinresistance. However, the effects of IF on fat in the pancreas and β-cell function remain largely unknown. Our aim was to evaluate the impact of IF on pancreatic fat accumulation and its effects on islet function.

METHODS:

New Zealand Obese (NZO) mice were fed a high-fat diet ad libitum (NZO-AL) or fasted every other day (intermittent fasting, NZO-IF) and pancreatic fat accumulation, glucose homoeostasis, insulin sensitivity, and islet function were determined and compared to ad libitum-fed B6.V-Lepob/ob (ob/ob) mice. To investigate the crosstalk of pancreatic adipocytes and islets, co-culture experiments were performed.

RESULTS:

NZO-IF mice displayed better glucose homeostasis and lower fat accumulation in both the pancreas (-32%) and the liver (-35%) than NZO-AL mice. Ob/ob animals were insulin-resistant and had low fat in the pancreas but high fat in the liver. NZO-AL mice showed increased fat accumulation in both organs and exhibited an impaired islet function. Co-culture experiments demonstrated that pancreatic adipocytes induced a hypersecretion of insulin and released higher levels of free fatty acids than adipocytes of inguinal white adipose tissue.

CONCLUSIONS:

These results suggest that pancreatic fat participates in diabetes development, but can be prevented byIF.

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