PMID- 23979788 OWN - NLM STAT- MEDLINE DCOM- 20140605 LR - 20220317 IS - 1439-4286 (Electronic) IS - 0018-5043 (Linking) VI - 45 IP - 11 DP - 2013 Oct TI - Serum preadipocyte factor-1 concentrations in females with obesity and type 2 diabetes mellitus: the influence of very low calorie diet, acute hyperinsulinemia, and fenofibrate treatment. PG - 820-6 LID - 10.1055/s-0033-1353210 [doi] AB - Appropriate differentiation capacity of adipose tissue significantly affects its ability to store lipids and to protect nonadipose tissues against lipid spillover and development of insulin resistance. Preadipocyte factor-1 (Pref-1) is an important negative regulator of preadipocyte differentiation. The aim of our study was to explore the changes in circulating Pref-1 concentrations in female subjects with obesity (OB) (n=19), females with obesity and type 2 diabetes mellitus (T2DM) (n=22), and sex- and age-matched healthy control subjects (C) (n=22), and to study its modulation by very low calorie diet (VLCD), acute hyperinsulinemia during isoglycemic-hyperinsulinemic clamp, and 3 months' treatment with PPAR-alpha agonist fenofibrate. At baseline, serum Pref-1 concentrations were significantly higher in patients with T2DM compared to control group, while only nonsignificant trend towards higher levels was observed in OB group. 3 weeks of VLCD decreased Pref-1 levels in both OB and T2DM group, whereas 3 months of fenofibrate treatment had no significant effect. Hyperinsulinemia during the clamp significantly suppressed Pref-1 levels in both C and T2DM subjects and this suppression was unaffected by fenofibrate treatment. In a combined population of all groups, circulating Pref-1 levels correlated positively with insulin, leptin and glucose levels and HOMA (homeostasis model assessment) index. We conclude that elevated Pref-1 concentrations in T2DM subjects may contribute to impaired adipose tissue differentiation capacity associated with insulin resistance in obese patients with T2DM. The decrease of Pref-1 levels after VLCD may be involved in the improvement of metabolic status and the amelioration of insulin resistance in T2DM patients. CI - (c) Georg Thieme Verlag KG Stuttgart . New York. FAU - Kavalkova, P AU - Kavalkova P AD - Third Department of Medicine, General University Hospital and First Faculty of Medicine, Charles University, Prague, Czech Republic. FAU - Touskova, V AU - Touskova V FAU - Roubicek, T AU - Roubicek T FAU - Trachta, P AU - Trachta P FAU - Urbanova, M AU - Urbanova M FAU - Drapalova, J AU - Drapalova J FAU - Haluzikova, D AU - Haluzikova D FAU - Mraz, M AU - Mraz M FAU - Novak, D AU - Novak D FAU - Matoulek, M AU - Matoulek M FAU - Lacinova, Z AU - Lacinova Z FAU - Haluzik, M AU - Haluzik M LA - eng PT - Clinical Trial PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20130826 PL - Germany TA - Horm Metab Res JT - Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme JID - 0177722 RN - 0 (Calcium-Binding Proteins) RN - 0 (DLK1 protein, human) RN - 0 (Intercellular Signaling Peptides and Proteins) RN - 0 (Membrane Proteins) RN - 0 (PPAR alpha) RN - U202363UOS (Fenofibrate) SB - IM MH - Anthropometry MH - Body Weight MH - Calcium-Binding Proteins MH - *Caloric Restriction MH - Diabetes Mellitus, Type 2/*blood/complications/*drug therapy MH - Female MH - Fenofibrate/*therapeutic use MH - Glucose Clamp Technique MH - Humans MH - Hyperinsulinism/*blood/drug therapy MH - Intercellular Signaling Peptides and Proteins/*blood MH - Membrane Proteins/*blood MH - Middle Aged MH - Obesity/*blood/complications/*diet therapy/drug therapy MH - PPAR alpha/agonists/metabolism EDAT- 2013/08/28 06:00 MHDA- 2014/06/06 06:00 CRDT- 2013/08/28 06:00 PHST- 2013/08/28 06:00 [entrez] PHST- 2013/08/28 06:00 [pubmed] PHST- 2014/06/06 06:00 [medline] AID - 10.1055/s-0033-1353210 [doi] PST - ppublish SO - Horm Metab Res. 2013 Oct;45(11):820-6. doi: 10.1055/s-0033-1353210. Epub 2013 Aug 26.