Gastrointestinal hormones play an important role in the neuroendocrine regulation of food intake and postprandial satiety. Ghrelin is a 28-amino acid orexigenic peptide produced mainly by the stomach that is involved in both the long-term regulation of body weight and the short-term regulation of postprandial satiety. Impairments in ghrelin secretion may in concert with other factors play an important role in the development of both obesity and anorexia nervosa. Despite an intensive research the critical factors regulating physiological postprandial ghrelin response in healthy individuals and its modification by the presence of obesity and anorexia nervosa are only partially understood. The potential contribution of ghrelin to the differences of diet- vs. surgical-induced weight losses in morbidly obese patients is now also being recognized. The aim of this review is to summarize the current knowledge about the physiology and pathophysiology of ghrelin and to discuss its potential in the prevention and/or treatment of obesity and anorexia nervosa.
Fibroblast growth factor 21 (FGF21) is a novel metabolic regulator produced primarily by the liver that exerts potent antidiabetic and lipid-lowering effects in animal models of obesity and type 2 diabetes mellitus. This hormone contributes to body weight regulation and is strongly involved in the response to nutritional deprivation and ketogenic state in mice. The principal sites of metabolic actions of FGF21 are adipose tissue, liver and pancreas. Experimental studies have shown marked improvements in diabetes compensation and dyslipidemia after FGF21 administration in diabetic mice and primates. Positive metabolic actions of FGF21 without the presence of apparent side effects make this factor a hot candidate to treat type 2 diabetes and accompanying metabolic diseases. The aim of this review is to summarize the current knowledge about the metabolic effects of FGF21 including some preliminary data on changes of its levels in humans with a special emphasis on its therapeutic potential in type 2 diabetes mellitus.
- MeSH
- diabetes mellitus 2. typu farmakoterapie metabolismus MeSH
- energetický metabolismus účinky léků MeSH
- fibroblastové růstové faktory metabolismus terapeutické užití účinky léků MeSH
- financování organizované MeSH
- hypoglykemika škodlivé účinky terapeutické užití MeSH
- látky proti obezitě škodlivé účinky terapeutické užití MeSH
- lidé MeSH
- modely nemocí na zvířatech MeSH
- obezita farmakoterapie metabolismus MeSH
- signální transdukce účinky léků MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
OBJECTIVE: Macrophage inhibitory cytokine-1 (MIC-1) is a novel regulator of energy homeostasis. We explored whether alterations in MIC-1 levels contribute to metabolic disturbances in patients with obesity and/or obesity and type 2 diabetes mellitus (T2DM). DESIGN: We measured serum MIC-1 levels and its mRNA expression in subcutaneous and visceral adipose tissue of 17 obese nondiabetic women, 14 obese women with T2DM and 23 healthy lean women. We also explored the relationship of MIC-1 with anthropometric and biochemical parameters and studied the influence of 2-week very low calorie diet (VLCD) on serum MIC-1 levels. METHODS: Serum MIC-1 levels were measured by ELISA and its mRNA expression was determined by RT-PCR. RESULTS: Both obese and T2DM group had significantly elevated serum MIC-1 levels relative to controls. T2DM group had significantly higher serum MIC-1 levels relative to obese group. Serum MIC-1 positively correlated with body weight, body fat, and serum levels of triglycerides, glucose, HbAlc, and C-reactive protein and it was inversely related to serum high-density lipoprotein cholesterol. Fat mRNA MIC-1 expression did not significantly differ between lean and obese women but it was significantly higher in subcutaneous than in visceral fat in both groups. VLCD significantly increased serum MIC-1 levels in obese but not T2DM group. CONCLUSION: Elevated MIC-1 levels in patients with obesity are further increased by the presence of T2DM. We suggest that in contrast to patients with cancer cachexia, increased MIC-1 levels in obese patients and diabetic patients do not induce weight loss.
- MeSH
- diabetes mellitus 2. typu dietoterapie genetika krev MeSH
- dieta MeSH
- dospělí MeSH
- hmotnostní úbytek genetika MeSH
- hubenost genetika metabolismus MeSH
- kalorická restrikce MeSH
- lidé středního věku MeSH
- lidé MeSH
- messenger RNA metabolismus MeSH
- obezita dietoterapie genetika krev MeSH
- růstový diferenciační faktor 15 genetika krev metabolismus MeSH
- tělesná hmotnost fyziologie MeSH
- tuková tkáň metabolismus MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- ženské pohlaví MeSH
- Publikační typ
- klinické zkoušky kontrolované MeSH
- práce podpořená grantem MeSH
OBJECTIVE: Adipose tissue-derived factors represent important players in the metabolic regulations acting both on systemic and local level. However, their local concentrations in human adipose tissue are poorly described. METHODS: We measured 24-hour profile and post-glucose load concentrations of selected adipokines in the subcutaneous adipose tissue of 17 healthy women by in vivo microdialysis. During 24-hour period, subjects consumed two standardized meals (at 13.00 h and at 19.00 h). RESULTS: During 24-hour period, fat interleukin-6, interleukin-8/CXCL8, resistin, and hepatocyte growth factor (HGF) exhibited increase/decrease/plateau pattern and peaked at about 14.30 h. Fat leptin exhibited increase/plateau/decrease/increase pattern and reached plateau between 22.00 and 5.30 h. Fat adiponectin exhibited decrease/plateau pattern and reached plateau between 1.00 and 7.00 h. Fat plasminogen activator inhibitor-1 (PAI-1) exhibited decrease/increase pattern with the lowest value at 20.30 h. Oral glucose consumption significantly increased fat adiponectin and resistin levels and decreased fat leptin and PAI-1 levels, respectively. CONCLUSIONS: The levels of studied adipokines in subcutaneous fat exhibited significant variations during the 24-hour period after microdialysis catheter insertion that were not reflected in the circulation. Concentrations of adiponectin, resistin, leptin and PAI-1 were regulated by oral glucose ingestion from 1 to 3 h after oral glucose load in healthy women.
- MeSH
- adipokiny MeSH
- adiponektin metabolismus MeSH
- glukosa metabolismus MeSH
- inhibitor aktivátoru plazminogenu 1 metabolismus MeSH
- interleukin-6 metabolismus MeSH
- interleukin-8 metabolismus MeSH
- leptin metabolismus MeSH
- lidé MeSH
- mikrodialýza metody MeSH
- mladý dospělý MeSH
- podkožní tuk metabolismus MeSH
- resistin metabolismus MeSH
- Check Tag
- lidé MeSH
- mladý dospělý MeSH
- ženské pohlaví MeSH
- Publikační typ
- klinické zkoušky MeSH
- práce podpořená grantem MeSH
Visfatin is an adipose tissue-derived hormone shown to correlate with visceral fat mass in patients with obesity. Its possible role in patients with different types of eating disorders is unknown. We measured fasting serum levels of visfatin and leptin and surrogate measures of insulin sensitivity in 10 untreated patients with anorexia nervosa (AN), 10 untreated patients with bulimia nervosa (BN) and 20 age-matched healthy women (C) to study the possible role of visfatin in these disorders. Patients with AN had severely decreased body mass index (BMI) and body fat content. BMI of BN group did not significantly differ from that of C group, whereas body fat content of BN group was significantly lower compared to C and higher compared to AN group, respectively. Serum glucose levels did not significantly differ among the groups studied, whereas serum insulin and leptin levels and HOMA index were significantly decreased in AN group relative to both C and BN group. In contrast, serum visfatin levels in both patients with AN and BN did not differ from those of C group. We conclude that circulating visfatin levels are not affected by the presence of chronic malnutrition in AN or binge/purge eating behavior in BN.
- MeSH
- adipozita MeSH
- biologické markery krev MeSH
- bulimia nervosa krev patofyziologie MeSH
- cytokiny MeSH
- dospělí MeSH
- financování organizované MeSH
- index tělesné hmotnosti MeSH
- inzulin krev MeSH
- krevní glukóza metabolismus MeSH
- leptin krev MeSH
- lidé MeSH
- mentální anorexie krev patofyziologie MeSH
- mladý dospělý MeSH
- nikotinamidfosforibosyltransferasa krev MeSH
- nutriční stav MeSH
- Check Tag
- dospělí MeSH
- lidé MeSH
- mladý dospělý MeSH
- ženské pohlaví MeSH
CONTEXT: Fibroblast growth factor 19 (FGF19) and FGF21 are novel metabolic regulators that improve insulin sensitivity and decrease adiposity in mice. However, little is known about the nutritional regulation of these factors in humans. OBJECTIVE: The objective of this study was to measure plasma FGF19 and FGF21 levels in patients with anorexia nervosa (AN) and to explore its relationship with anthropometric and endocrine parameters. DESIGN: This was a single-center cross-sectional study. SETTING: The study was performed in a university hospital. PATIENTS: Seventeen untreated women with a restrictive type of AN and 17 healthy women (control group) were included. MAIN OUTCOME MEASURES: Fasting plasma FGF19 and FGF21, serum insulin, leptin, soluble leptin receptor, adiponectin, resistin, and C-reactive protein were the main outcome measures. RESULTS: Plasma FGF19 levels did not significantly differ between the groups studied, whereas plasma FGF21 levels were significantly reduced in AN relative to the control group. Plasma FGF21 positively correlated with body mass index and serum leptin and insulin and was inversely related to serum adiponectin in both groups. In contrast, plasma FGF19 was not related to any of parameters studied. Partial realimentation significantly reduced plasma FGF21 levels in AN. CONCLUSION: Circulating levels of FGF21 but not FGF19 are strongly related to body weight and serum levels of leptin, adiponectin, and insulin in both anorectic and normal-weight women. We suggest that reduced plasma FGF21 levels could be involved in the pathophysiology of AN or in a complex adaptive response to this disease.
- MeSH
- adiponektin krev MeSH
- biologická adaptace fyziologie MeSH
- dospělí MeSH
- fibroblastové růstové faktory fyziologie krev MeSH
- financování organizované MeSH
- index tělesné hmotnosti MeSH
- inzulin krev MeSH
- leptin krev MeSH
- lidé MeSH
- mentální anorexie etiologie krev MeSH
- přijímání potravy fyziologie MeSH
- průřezové studie MeSH
- studie případů a kontrol MeSH
- tělesná hmotnost fyziologie MeSH
- trijodthyronin krev MeSH
- Check Tag
- dospělí MeSH
- lidé MeSH
- ženské pohlaví MeSH
- Publikační typ
- klinické zkoušky MeSH
