Brain-gut microbiota interactions are intensively studied in connection with various neurological and psychiatric diseases. While anorexia nervosa (AN) pathophysiology is not entirely clear, it is presumably linked to microbiome dysbiosis. We aimed to elucidate the gut microbiota contribution in AN disease pathophysiology. We analyzed the composition and diversity of the gut microbiome of patients with AN (bacteriome and mycobiome) from stool samples before and after renourishment, and compared them to healthy controls. Further, levels of assorted neurotransmitters and short-chain fatty acids (SCFA) were analyzed in stool samples by MS and NMR, respectively. Biochemical, anthropometric, and psychometric profiles were assessed. The bacterial alpha-diversity parameter analyses revealed only increased Chao 1 index in patients with AN before the realimentation, reflecting their interindividual variation. Subsequently, core microbiota depletion signs were observed in patients with AN. Overrepresented OTUs (operation taxonomic units) in patients with AN taxonomically belonged to Alistipes, Clostridiales, Christensenellaceae, and Ruminococcaceae. Underrepresented OTUs in patients with AN were Faecalibacterium, Agathobacter, Bacteroides, Blautia, and Lachnospira. Patients exhibited greater interindividual variation in the gut bacteriome, as well as in metagenome content compared to controls, suggesting altered bacteriome functions. Patients had decreased levels of serotonin, GABA, dopamine, butyrate, and acetate in their stool samples compared to controls. Mycobiome analysis did not reveal significant differences in alpha diversity and fungal profile composition between patients with AN and healthy controls, nor any correlation of the fungal composition with the bacterial profile. Our results show the changed profile of the gut microbiome and its metabolites in patients with severe AN. Although therapeutic partial renourishment led to increased body mass index and improved psychometric parameters, SCFA, and neurotransmitter profiles, as well as microbial community compositions, did not change substantially during the hospitalization period, which can be potentially caused by only partial weight recovery.
- MeSH
- Archaea klasifikace růst a vývoj MeSH
- Bacteria klasifikace růst a vývoj metabolismus MeSH
- dospělí MeSH
- feces mikrobiologie MeSH
- houby klasifikace růst a vývoj metabolismus MeSH
- index tělesné hmotnosti MeSH
- kyseliny mastné těkavé metabolismus MeSH
- lidé MeSH
- longitudinální studie MeSH
- mentální anorexie metabolismus mikrobiologie MeSH
- metagenom MeSH
- mladý dospělý MeSH
- mykobiom MeSH
- neurotransmiterové látky metabolismus MeSH
- osa mozek-střevo MeSH
- střevní mikroflóra * MeSH
- Check Tag
- dospělí MeSH
- lidé MeSH
- mladý dospělý MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Adipose tissue is recognized as an active endocrine organ that produces a number of endocrine substances referred to as "adipokines" including leptin, adiponectin, adipolin, visfatin, omentin, tumour necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), resistin, pigment epithelium-derived factor (PEDF), and progranulin (PGRN) which play an important role in the food intake regulation and significantly influence insulin sensitivity and in some cases directly affect insulin resistance in skeletal muscle, liver, and adipose tissue. The review summarizes current knowledge about adipose tissue-derived hormones and their influence on energy homeostasis regulation. The possible therapeutic potential of these adipokines in the treatment of insulin resistance, endothelial dysfunction, a pro-inflammatory response, obesity, eating disorders, progression of atherosclerosis, type 1 diabetes, and type 2 diabetes is discussed.
- MeSH
- adipokiny fyziologie MeSH
- buněčné mikroprostředí fyziologie MeSH
- energetický metabolismus fyziologie MeSH
- energetický příjem fyziologie MeSH
- homeostáza fyziologie MeSH
- inzulinová rezistence fyziologie MeSH
- lidé MeSH
- tuková tkáň sekrece MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- přehledy MeSH
- Klíčová slova
- visfatin, TNF-?, interleukin 6,
- MeSH
- adipokiny fyziologie metabolismus MeSH
- adiponektin fyziologie metabolismus MeSH
- interleukiny fyziologie metabolismus MeSH
- leptin fyziologie metabolismus MeSH
- lidé MeSH
- nikotinamidfosforibosyltransferasa fyziologie metabolismus MeSH
- resistin fyziologie metabolismus MeSH
- Check Tag
- lidé MeSH
OBJECTIVE: Ghrelin is predominantly produced by the stomach and the growth hormone (GH)-ghrelin feedback loop between the stomach and the pituitary gland has recently been suggested. The disruption of the gut-brain axis might be involved in bulimia nervosa (BN). METHODS: We investigated responses of plasma GH, ghrelin, and neuropeptide Y (NPY) concentrations to exercise or to exercise after the administration of the antilipolytic drug Acipimox (Aci) in seven BN patients and seven healthy women (C). Aci was administered 1h before exercise (45 min, 2 W/kg of lean body mass/LBM/). Ghrelin, GH, NPY, free fatty acids (FFA) and glycerol plasma levels were measured during the test using commercial kits. RESULTS: The exercise induced an increase in plasma GH, NPY and FFA in both groups and a decrease in plasma ghrelin levels only in BN patients. Exercise after Aci administration resulted in an increase in plasma GH, and a decrease in plasma ghrelin in both groups; NPY increased more in BN patients. Exercise-induced FFA increase was depressed after Aci. CONCLUSIONS: We conclude that the Aci-induced suppression in plasma ghrelin levels during exercise in both groups suggests a negative feedback of GH on ghrelin secretion. Observed changes in plasma FFA levels were not related to changes in GH and ghrelin levels.
- MeSH
- bulimia nervosa krev patofyziologie MeSH
- cvičení fyziologie MeSH
- dospělí MeSH
- experimenty na lidech MeSH
- ghrelin biosyntéza sekrece MeSH
- glycerol krev MeSH
- hypofýza účinky léků sekrece MeSH
- hypolipidemika aplikace a dávkování MeSH
- index tělesné hmotnosti MeSH
- kyseliny mastné neesterifikované krev MeSH
- lidé MeSH
- lidský růstový hormon biosyntéza sekrece MeSH
- neuropeptid Y krev MeSH
- pyraziny aplikace a dávkování MeSH
- studie případů a kontrol MeSH
- žaludek účinky léků metabolismus MeSH
- zpětná vazba fyziologická MeSH
- Check Tag
- dospělí MeSH
- lidé MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Anorexia nervosa (AN) is characterized by self-induced starvation leading to severe weight and fat loss. In the present study, we measured fasting plasma levels of adiponectin, leptin, resistin, insulin and glucose in 10 women with a restrictive type of AN and in 12 healthy women (C). Insulin sensitivity was determined according to homeostasis model assessment of insulin resistance (HOMA-R). Plasma resistin, leptin and insulin levels were significantly decreased, whereas plasma adiponectin levels were significantly increased in patients with AN compared to the C. HOMA-R was significantly decreased in patients with AN compared to the C group. Plasma adiponectin and leptin concentrations negatively and positively correlated with the body mass index and percentage body fat in both groups. Plasma adiponectin levels were negatively related to plasma insulin levels in the AN group only. In conclusion, we demonstrated that AN is associated with significantly decreased plasma leptin and resistin levels, markedly increased plasma adiponectin levels and increased insulin sensitivity. Plasma leptin and adiponectin levels were related to the body size and adiposity. Hyperadiponectinemia could play a role in increased insulin sensitivity of patients with AN. Neither body size and adiposity nor insulin sensitivity are the major determinants of plasma resistin levels in AN.
- MeSH
- adipokiny izolace a purifikace krev metabolismus MeSH
- adiponektin izolace a purifikace krev metabolismus MeSH
- financování organizované využití MeSH
- index tělesné hmotnosti MeSH
- interpretace statistických dat MeSH
- inzulinová rezistence fyziologie MeSH
- mentální anorexie komplikace metabolismus MeSH
- resistin izolace a purifikace krev metabolismus MeSH
- ženy MeSH
