Dissociation between adipose tissue expression and serum levels of adiponectin during and after diet-induced weight loss in obese subjects with and without the metabolic syndrome.
The study aimed to examine if dysmetabolic subjects (MetS+) have lower adiponectin gene expression and lower circulating adiponectin levels than non-dysmetabolic obese subjects (MetS-) at baseline, if adiponectin expression and adiponectin concentration rise more in the dysmetabolic group during weight loss, and if v-SNARE Vti1a (vesicle transport soluble NSF attachment protein receptor vps10p tail interacting 1a) expression increases during the weight loss, as a mechanism for increased adiponectin secretion. Twenty-one obese MetS+ and 19 obese MetS- subjects underwent a very low-energy diet for 16 weeks followed by 2 weeks of refeeding. Abdominal subcutaneous adipose tissue biopsies and blood samples were taken before, during, and after dieting for DNA microarray, reverse transcriptase-polymerase chain reaction, and biochemical analyses. Serum adiponectin was also assessed in a sex- and age-matched healthy, nonobese reference group. Weight decreased by 26.3+/-9.8 kg in the MetS+ group and 28.2+/-8.4 kg in the MetS- group with concomitant reductions in insulin, hemoglobin A1c, and triglycerides that were more pronounced in the MetS+ group. Initially, the MetS+ subjects had lower serum adiponectin, but the differences disappeared at week 8, with a continuous increase in serum adiponectin throughout the study in both groups to a level that was higher than in the reference group. The expression of adiponectin and v-SNARE Vti1a did not differ between the groups or over time. In conclusion, obese subjects with the metabolic syndrome had lower circulating adiponectin than subjects without the syndrome. Weight loss increased serum levels of adiponectin without a parallel increase in adiponectin gene expression. The mechanisms involved in the regulation of adiponectin levels merits further investigation.
Behre
Carl Johan
CJ
Wallenberg Laboratory for Cardiovascular Research, Institute of Medicine, The Sahlgrenska Academy, Göteborg University, SE-413 45 Göteborg, Sweden.
Gummesson
Anders
A
Jernås
Margareta
M
Lystig
Theodore C
TC
Fagerberg
Björn
B
Carlsson
Björn
B
Carlsson
Lena M S
LM
D052242:Adiponectin / Q000096:biosynthesis* / Q000097:blood*; D000273:Adipose Tissue / Q000378:metabolism* / Q000473:pathology; D000328:Adult; D001835:Body Weight / Q000502:physiology; D004038:Diet, Reducing; D002149:Energy Intake / Q000502:physiology; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D015870:Gene Expression / Q000502:physiology; D006442:Glycated Hemoglobin / Q000378:metabolism; D006801:Humans; D007328:Insulin / Q000097:blood; D020738:Leptin / Q000097:blood; D008297:Male; D024821:Metabolic Syndrome / Q000150:complications / Q000178:diet therapy* / Q000378:metabolism*; D008875:Middle Aged; D009765:Obesity / Q000150:complications / Q000178:diet therapy* / Q000378:metabolism*; D020411:Oligonucleotide Array Sequence Analysis; D012313:RNA / Q000096:biosynthesis / Q000302:isolation & purification; D020133:Reverse Transcriptase Polymerase Chain Reaction; D050600:SNARE Proteins / Q000235:genetics / Q000502:physiology; D014280:Triglycerides / Q000097:blood; D015431:Weight Loss / Q000502:physiology*
D052242:Adiponectin; D006442:Glycated Hemoglobin; D007328:Insulin; D020738:Leptin; D012313:RNA; D050600:SNARE Proteins; D014280:Triglycerides