Contribution of individual adiponectin isoforms to lipolysis regulation remains unknown. We investigated the impact of full-length, trimeric and globular adiponectin isoforms on spontaneous lipolysis in subcutaneous abdominal (SCAAT) and visceral adipose tissues (VAT) of obese and non-obese subjects. Furthermore, we explored the role of AMPK (5'-AMP-activated protein kinase) in adiponectin-dependent lipolysis regulation and expression of adiponectin receptors type 1 and 2 (AdipoR1 and AdipoR2) in SCAAT and VAT. Primary adipocytes isolated from SCAAT and VAT of obese and non-obese women were incubated with 20 µg/ml of: A) full-length adiponectin (physiological mixture of all adiponectin isoforms), B) trimeric adiponectin isoform or C) globular adiponectin isoform. Glycerol released into media was used as a marker of lipolysis. While full-length adiponectin inhibited lipolysis by 22% in non-obese SCAAT, globular isoform inhibited lipolysis by 27% in obese SCAAT. No effect of either isoform was detected in non-obese VAT, however trimeric isoform inhibited lipolysis by 21% in obese VAT (all p<0.05). Trimeric isoform induced Thr172 p-AMPK in differentiated preadipocytes from a non-obese donor, while globular isoform induced Ser79 p-ACC by 32% (p<0.05) and Ser565 p-HSL by 52% (p = 0.08) in differentiated preadipocytes from an obese donor. AdipoR2 expression was 17% and 37% higher than AdipoR1 in SCAAT of obese and non-obese groups and by 23% higher in VAT of obese subjects (all p<0.05). In conclusion, the anti-lipolytic effect of adiponectin isoforms is modified with obesity: while full-length adiponectin exerts anti-lipolytic action in non-obese SCAAT, globular and trimeric isoforms show anti-lipolytic activity in obese SCAAT and VAT, respectively.

• MeSH
• adiponektin krev   chemie   metabolismus   MeSH
• aminoimidazolkarboxamid analogy a deriváty   farmakologie   MeSH
• dospělí MeSH
• exprese genu účinky léků   MeSH
• hypoglykemika farmakologie   MeSH
• kultivované buňky MeSH
• kvantitativní polymerázová řetězová reakce MeSH
• lidé středního věku MeSH
• lidé MeSH
• lipolýza účinky léků   MeSH
• multimerizace proteinu účinky léků   MeSH
• nitrobřišní tuk cytologie   MeSH
• obezita patologie   MeSH
• podkožní tuk cytologie   MeSH
• protein - isoformy krev   chemie   metabolismus   MeSH
• proteinkinasy aktivované AMP metabolismus   MeSH
• receptory adiponektinu genetika   metabolismus   MeSH
• ribonukleotidy farmakologie   MeSH
• tukové buňky cytologie   účinky léků   metabolismus   MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• adiponektin MeSH
• ADIPOR1 protein, human MeSH Prohlížeč
• ADIPOR2 protein, human MeSH Prohlížeč
• AICA ribonucleotide MeSH Prohlížeč
• aminoimidazolkarboxamid MeSH
• hypoglykemika MeSH
• protein - isoformy MeSH
• proteinkinasy aktivované AMP MeSH
• receptory adiponektinu MeSH
• ribonukleotidy MeSH

Calorie restriction-induced weight loss is accompanied by profound changes in adipose tissue characteristics. To determine the effect of weight loss on differentiation of preadipocytes and secretory capacity of in vitro differentiated adipocytes, we established cultures of these cells from paired subcutaneous adipose tissue biopsies obtained before and at the end of weight-reducing dietary intervention (DI) in 23 obese women. Based on lipid accumulation and the expression of differentiation markers, in vitro adipogenesis increased after weight loss and it was accompanied by enhanced expression of genes involved in de novo lipogenesis. This effect of weight loss was not driven by changes of peroxisome proliferator-activated receptor γ sensitivity to rosiglitazone. Weight loss also enhanced the expression of adiponectin and leptin while reducing that of monocyte chemoattractant protein 1 and interleukin-8 by cultured adipocytes. Thus, the weight-reducing (DI) increased adipogenic capacity of preadipocytes and shifted their secretion toward lower inflammatory profile. Reprogramming of preadipocytes could represent an adaptation to weight loss leading to partial restoration of preobese adipose tissue traits and thus contribute to the improvement of metabolic status. However, enhanced adipogenesis could also contribute to the unwanted weight regain after initial weight loss.

• MeSH
• adipogeneze genetika   fyziologie   MeSH
• adiponektin metabolismus   MeSH
• chemokin CCL2 metabolismus   MeSH
• cytokiny metabolismus   MeSH
• ELISA MeSH
• hmotnostní úbytek genetika   fyziologie   MeSH
• interleukin-8 metabolismus   MeSH
• kultivované buňky MeSH
• leptin metabolismus   MeSH
• lidé MeSH
• obezita MeSH
• PPAR gama metabolismus   MeSH
• rosiglitazon MeSH
• thiazolidindiony farmakologie   MeSH
• tukové buňky cytologie   MeSH
• Check Tag
• lidé MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• adiponektin MeSH
• chemokin CCL2 MeSH
• cytokiny MeSH
• interleukin-8 MeSH
• leptin MeSH
• PPAR gama MeSH
• rosiglitazon MeSH
• thiazolidindiony MeSH