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Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Pancreatic adipocytes mediate hypersecretion of insulin in diabetes-susceptible mice.
Metabolism 97, 9-17 (2019)
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 insulin resistance. However, the effects of IF on fat in the pancreas and beta-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-Lep(ob/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 adds than adipocytes of inguinal white adipose tissue.Conclusions: These results suggest that pancreatic fat participates in diabetes development, but can be prevented by IF.
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Publikationstyp
Artikel: Journalartikel
Dokumenttyp
Wissenschaftlicher Artikel
Schlagwörter
Beta-cell Function; Fatty Pancreas; Gene-expression; Ectopic Fat; Liver; Glucolipotoxicity; Resistance; Disease; Restriction
ISSN (print) / ISBN
0026-0495
e-ISSN
1532-8600
Zeitschrift
Metabolism: clinical and experimental
Quellenangaben
Band: 97,
Seiten: 9-17
Verlag
Elsevier
Verlagsort
1600 John F Kennedy Boulevard, Ste 1800, Philadelphia, Pa 19103-2899 Usa
Nichtpatentliteratur
Publikationen
Begutachtungsstatus
Peer reviewed