Abstract
Adipose tissue (AT) has a modulating role in obesity-induced metabolic complications like type 2 diabetes mellitus (T2DM) via the production of so-called adipokines such as leptin, adiponectin, and resistin. The adipokines are believed to influence other tissues and to affect insulin resistance, liver function, and to increase the risk of T2DM. In this study, we examined the impact of intervention with the short-chain fatty acid butyrate following a high-fat diet (HFD) on AT function and other metabolic risk factors associated with obesity and T2DM in mice during mid- and late life. In both mid- and late adulthood, butyrate reduced HFD-induced adipocyte hypertrophy and elevations in leptin levels, which were associated with body weight, and cholesterol and triglyceride levels. HFD feeding stimulated macrophage accumulation primarily in epididymal AT in both mid- and late life adult mice, which correlated with liver inflammation in late adulthood. In late-adult mice, butyrate diminished increased insulin levels, which were related to adipocyte size and macrophage content in epididymal AT. These results suggest that dietary butyrate supplementation is able to counteract HFD-induced detrimental changes in AT function and metabolic outcomes in late life. These changes underlie the obesity-induced elevated risk of T2DM, and therefore it is suggested that butyrate has potential to attenuate risk factors associated with obesity and T2DM.
Highlights
In line with the rise of type 2 diabetes mellitus (T2DM) the global prevalence of obesity has more than doubled since 1980 [1]
As follow-up of the previous published study [18], we investigated in the current study the effects of a therapeutic butyrate intervention on adipose tissue function and adipokine levels in the context of manifested high-fat diet (HFD)-induced obesity in both mid- and late-adult LDLr-/-.Leiden mice
Mean inguinal adipocyte size was significantly larger in late adult as compared to mid-adult high fat diet enriched with butyrate (HFDB) mice (p < 0.01; F(1,18) = 11.28)
Summary
In line with the rise of type 2 diabetes mellitus (T2DM) the global prevalence of obesity has more than doubled since 1980 [1]. Obesity is a major risk factor for T2DM, accounting for 80–85% of the overall risk [2]. It has been suggested that the relationship between obesity and T2DM exists already at a young age [4,5,6]. Obesity is suggested to exaggerate aging processes [7], and aging is associated with impaired insulin signaling [8], which causes an increase in blood glucose levels. High blood glucose concentrations combined with high blood pressure and high cholesterol levels affect vascular function, and may evolve into cardiovascular disease, kidney failure, and subsequent cognitive deficits [9,10]
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