Abstract
Background and aimsGroup 2 innate lymphoid cells (ILC2s) have been implicated in the regulation of metabolic homeostasis in mice.MethodsIn this study, the role of ILC2s in white adipose tissue (WAT) was investigated using ST2, an IL-33 receptor that is expressed on ILC2 knockout mice.ResultsThe deficiency of ST2 decreased ILC2s in WAT, whereas ex-ILC2, which acquired group 1 innate lymphoid cell (ILC1)-like traits, was increased. This led to significant metabolic disorders such as visceral fat obesity, decreased browning in WAT, reduction of energy metabolism, and impaired glucose tolerance, compared to wild type (WT) mice. Those metabolic abnormalities of ST2-knockout (ST2KO) mice were not ameliorated by IL-33 administration, but impaired glucose tolerance and visceral fat obesity were significantly improved by transplantation of ILCs from the bone marrow of WT mice. The relative expression of Cd36 in WAT increased due to the deficiency of ST2, and the storage of saturated fatty acids in WAT of ST2KO mice was significantly higher than that of WT mice. Moreover, saturated fatty acids aggravated the chronic inflammation in adipocytes, promoted the differentiation of M1-like macrophages, and inhibited that of M2-like macrophages.ConclusionsOur results indicated that ILC2 regulates diet-induced obesity and chronic inflammation through the regulation of saturated fatty acid absorption in visceral adipose tissue.
Highlights
The number of patients with type 2 diabetes mellitus has been increasing worldwide [1]
On the other hand, fasting blood glucose levels and area under the curve (AUC) of intraperitoneal glucose tolerance test (iPGTT) in ST2KO mice at 20-week old were significantly higher than those in WT mice (Figures 1C–E), and ST2KO mice fed with high-fat highsucrose diet (HFHSD) showed decreased insulin sensitivity compared to WT mice fed with HFHSD (p = 0.002) (Figures 1F, G)
The Number of ILC2s Decreased in WT Mice Fed a HFHSD, Whereas the Decrease of ILC2s Did Not Show in ST2KO Mice
Summary
The number of patients with type 2 diabetes mellitus has been increasing worldwide [1]. It is well known that obesity has a close association with type 2 diabetes. The world’s obese population has increased rapidly in 40 years since 1975, reaching 641 million affected people [2], and this is one of the reasons that the incidence of type 2 diabetes is rapidly increasing. The causes of obesity are lack of exercise [3], lack of sleep or poor quality of sleep [4], and excessive stress [5]; one of the main causes is excessive consumption of high-energy foods, especially those high in fat and sugar [6]. Excessive fat intake is a clear cause of obesity and has been shown to be an important factor in the development of diabetes [7]. Group 2 innate lymphoid cells (ILC2s) have been implicated in the regulation of metabolic homeostasis in mice
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