Abstract
PurposeObesity is characterized by insulin resistance and low-grade systemic and adipose tissue (AT) inflammation. It remains unclear whether beneficial effects of weight loss are related to AT inflammation. We aimed to assess the effect of weight loss during low-calorie diet on insulin sensitivity, AT expression of genes associated with inflammation in young subjects with obesity. Furthermore, we estimated the effects of immunomodulatory (1, 3)(1, 6)-β-glucan (BG) on the above parameters.MethodsThe study group comprised 52 subjects with obesity. Twelve-week dietary intervention was applied, with randomization to receive or not 500 mg BG daily. Euglycemic hyperinsulinemic clamp, subcutaneous AT biopsy were performed before and after the program. Twenty normal-weight subjects, examined at baseline, served as a control group.ResultsAt baseline, obese subjects had lower insulin sensitivity, lower AT ADIPOQ, JAK1, and JAK2 expression and higher AT expression of LEP, IL6ST, STAT3, MIF, CCL2, MMP9, and IL18. Forty obese subjects completed dietary intervention program, which resulted in 11.3% weight loss and 27% increase in insulin sensitivity (both p < 0.0001). AT IL6R, IL6ST, JAK1, and JAK2 expression increased, whereas MIF, CCL2, MMP9, and IL18 gene expression did not change in response to weight loss. BG addition had no effect on any of the parameters studied.ConclusionsOur data indicate that reduction in AT inflammation is not required for an improvement in insulin action during weight loss in subjects with uncomplicated obesity. BG does not have effects during dietary intervention.
Highlights
Obesity is associated with an increased risk of type 2 diabetes, dyslipidemia, hypertension, cardiovascular disease, different forms of cancer [1]
Glycoprotein 130 cytokines regulate inflammatory processes. This family comprises a group of proteins, Endocrine (2018) 61:275–284 which include interleukin 6 (IL-6) among others, that induce their signal through association with cell-surface transmembrane receptor and signal transduction membrane-bound gp130, known as IL-6 signal transducer (IL-6ST) [9], common for all cytokines
In our previous studies we demonstrated that sgp130 was inversely related to insulin action, which may suggest an inhibition of intracellular gp130 signaling in insulin-resistant conditions [12]
Summary
Obesity is associated with an increased risk of type 2 diabetes, dyslipidemia, hypertension, cardiovascular disease, different forms of cancer [1]. The main negative feedback regulator of the gp130 signaling is Suppressor of Cytokine Signaling 3 (SOCS3), which is a STAT3 target gene and is transcriptionally upregulated after cellular gp130 activation by IL-6 [10]. Both IL-6R and gp130 are present in the blood in the soluble forms (sIL-6R and sgp130, respectively). In our previous studies we demonstrated that sgp130 was inversely related to insulin action, which may suggest an inhibition of intracellular gp130 signaling in insulin-resistant conditions [12]. Little is known about the expression of gp130 signaling genes in metabolic tissues in humans, especially in AT
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
