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Metabolic status of adipocytes triggers rapid adjustments of systemic glucose tolerance
Author(s) -
Kless Caroline,
Klingenspor Martin
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1071.2
Subject(s) - medicine , endocrinology , anabolism , catabolism , adipose tissue , obesity , metabolism , diet induced obese , biology , energy metabolism , chemistry , insulin resistance
Adipose tissue expansion is one potential cause for impaired systemic glucose tolerance (GT). In three inbred mouse strains with different susceptibility to diet‐induced obesity (DIO) we monitored GT after high fat feeding and in response to caloric restriction. Male AKR/J, SWR/J and C57BL/6J mice received high‐fat diet (HFD, 48 kJ% fat) or control diet (CD, 12 kJ% fat) for 12 weeks, followed by either refeeding of CD or restricted pair‐feeding with HFD. Body mass, body composition, energy intake, energy expenditure and oral GT were measured regularly. Acutely, HFD feeding for 1.5 days increased energy intake and reduced GT in all three strains. During prolonged HFD feeding, DIO prone AKR/J and B/6J mice, but not DIO resistant SWR/J mice, maintained impaired GT. Refeeding CD or pair‐ feeding HFD of obese AKR/J mice normalized normalized GT rapidly. These results demonstrate that HFD triggers a fast reduction of GT, independent of DIO susceptibility. This is an acute metabolic response to the increased utilization of fatty acids as energy substrates. Impaired GT is only maintained in mouse strains prone to DIO suggesting an important contribution of anabolic metabolism of adipocytes whereas shifting towards a catabolic state of adipocytes rapidly normalizes GT. This work was supported by BMBF FKZ 0315674 to MK.