Monika Karczewska-Kupczewska, Agnieszka Nikołajuk, Magdalena Stefanowicz, Natalia Matulewicz, Irina Kowalska and Marek Strączkowski
The aim of the study was to assess serum chemerin concentration and s.c. adipose tissue (SAT) chemerin expression in relation to insulin sensitivity and obesity in young healthy subjects.
We performed a cross-sectional study including 128 subjects, 44 with normal weight, 44 with overweight and 40 with obesity.
Hyperinsulinemic-euglycemic clamp and SAT biopsy were performed. Next, 30 subjects with obesity underwent 12-week weight-reducing dietary intervention.
Serum chemerin was higher and SAT chemerin expression was lower in subjects with obesity in comparison with other groups. The relationship of serum chemerin with SAT expression and insulin sensitivity were positive in normal weight and overweight individuals, and negative in individuals with obesity. In the entire study population, serum chemerin was also positively related to hsCRP, serum fetuin A and alanine aminotransferase. SAT chemerin was positively related to insulin sensitivity, SAT insulin signaling and adipogenic genes. Weight loss decreased serum chemerin, whereas SAT chemerin increased in subjects with the highest increase in insulin sensitivity.
Serum and SAT chemerin is differentially associated with insulin sensitivity and the relationship between serum chemerin and insulin sensitivity depends on adiposity. SAT chemerin is positively associated with insulin sensitivity across a wide range of BMIs and may be proposed as a biomarker of metabolically healthy SAT. Our results suggest that SAT is not the main source of serum chemerin in obesity.
Monika Karczewska-Kupczewska, Agnieszka Nikołajuk, Radosław Majewski, Remigiusz Filarski, Magdalena Stefanowicz, Natalia Matulewicz and Marek Strączkowski
Insulin resistance is a major pathophysiological link between obesity and its metabolic complications. Weight loss (WL) is an effective tool to prevent obesity-related diseases; however, the mechanisms of an improvement in insulin sensitivity (IS) after weight-reducing interventions are not completely understood. The aim of the present study was to analyze the relationships between IS and adipose tissue (AT) expression of the genes involved in the regulation of lipolysis in obese subjects after WL.
Fifty-two obese subjects underwent weight-reducing dietary intervention program. The control group comprised 20 normal-weight subjects, examined at baseline only. Hyperinsulinemic-euglycemic clamp and s.c. AT biopsy with subsequent gene expression analysis were performed before and after the program.
AT expression of genes encoding lipases (PNPLA2, LIPE and MGLL) and lipid-droplet proteins enhancing (ABHD5) and inhibiting lipolysis (PLIN1 and CIDEA) were decreased in obese individuals in comparison with normal-weight individuals. The group of 38 obese participants completed dietary intervention program and clamp studies, which resulted in a significant WL and an improvement in mean IS. However, in nine subjects from this group IS did not improve in response to WL. AT expression of PNPLA2, LIPE and PLIN1 increased only in the group without IS improvement.
Excessive lipolysis may prevent an improvement in IS during WL. The change in AT PNPLA2 and LIPE expression was a negative predictor of the change in IS after WL.