Abstract
Dysfunctional adipose tissue phenotype underpins type 2 diabetes mellitus (T2DM) development. The disruption of circadian rhythms contributes to T2DM development. We investigated the effects of high-energy diet and photoperiod length on visceral and subcutaneous adipose tissue phenotype. Psammomys obesus sand rats exposed to neutral (12 light:12 dark) or short (5 light:19 dark) photoperiod were fed a low- (LE) or high- (HE) energy diet. The HE diet and/or short photoperiod reduced subcutaneous expression of adipocyte differentiation/function markers C/ebpα, Pparδ, Pparγ and Adipoq. Visceral Pparα levels were elevated in the 5:19HE group; however, the HE diet and/or short photoperiod decreased visceral Pparγ and Adipoq expression. 5:19HE animals had elevated Ucp1 yet lower Pgc-1α levels. The HE diet increased visceral Tgf-β1, Ccl2 and Cd68 levels, suggestive of a pro-inflammatory state. Daily visceral rhythms of these genes were affected by a short photoperiod and/or HE diet. The 12:12HE, 5:19LE or 5:19HE animals had a higher proportion of larger adipocytes, indicating increased adipocyte hypertrophy. Collectively, the HE diet and/or shorter light exposure drives a dysfunctional adipose tissue phenotype. Daily rhythms are affected by a short photoperiod and HE diet in a site-specific manner. These findings provide mechanistic insight on the influence of disrupted circadian rhythms and HE diet on adipose tissue phenotype.
Highlights
Adipose tissue metabolism is closely linked to insulin resistance and variations in fat distribution are associated with type 2 diabetes mellitus (T2DM) [1]
We found that a high-energy diet and short photoperiod drives features characteristic of a dysfunctional adipose tissue phenotype
We find that C/EBPα and PPARγ expression are driven by HE diet, short photoperiod or the combination of both in a site-dependent manner; with C/ebpα levels being strikingly inhibited in the subcutaneous adipose tissue while in the visceral adipose tissue, Pparγ was reduced, suggesting that adipocyte differentiation is impaired and driven by different transcription factors under these conditions
Summary
Adipose tissue metabolism is closely linked to insulin resistance and variations in fat distribution are associated with T2DM [1]. This study sought to determine whether high-energy diet, in combination with a disrupted circadian rhythm, contribute to gene and phenotypic changes reflective of dysfunctional adipose tissue including insulin-resistant adipocytes, a pro-inflammatory milieu and adipocyte hypertrophy. We hypothesized that short photoperiod would exacerbate the detrimental effects of the high-energy diet, driving an insulin-resistant and pro-inflammatory adipose tissue phenotype. We found that a high-energy diet and short photoperiod drives features characteristic of a dysfunctional adipose tissue phenotype. This includes elevated pro-inflammatory marker expression and increased adipocyte hypertrophy, which is associated with the development of T2DM. Short photoperiod and high-energy diet strikingly affected daily rhythms in the visceral adipose depot, a key contributor to whole body insulin resistance. Photoperiod denoted by light:dark hours 12:12, neutral; 5:19, short; LE, low-energy diet; HE, highenergy diet
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