Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Background: Hyperadiponectinemia is an indicator of worse outcomes in advanced heart failure (HF), its role in de novo HF is less clear. Objective: Because this protein is a hormone with starvation properties, we wanted to know its association with nutritional state and its regulator factors in de novo HF. Methods: Adiponectin circulating levels were determined by ELISA at discharge in patients admitted for de novo HF (n=74). Nutritional status was determined by CONUT score. Univariate and multivariate Cox regression analyses were employed to calculate the estimated hazard ratio (HR) with 95% confidence interval (CI) for death or all-cause readmission. Stromal vascular cells (SVC) of EAT and subcutaneous adipose tissue (SAT) from patients (n=5) underwent heart surgery were induced to adipogenesis for 18 days. Then, cells were cultured with complete or starved medium for 8 hours. At the end, adiponectin expression levels were analysed by real time polymerase chain reaction. Results: Patients were grouped regarding nutritional status. There was a strong association between high adiponectin levels and failing nutritional status. Those patients with worse nutritional state had the highest adiponectin and proBNP levels at discharge (p<0.01). Both proteins were slightly correlated (p<0.05). However, only high adiponectin levels were independently associated with death or all-cause readmission. Nutrients starvation upregulated adiponectin expression levels in adipogenesis-induced SVC from EAT or SAT. Conclusions: Worse nutritional state in de novo HF patients is associated with higher adiponectin plasma levels. Their levels were upregulated in adipose cells after being nutrients-starved. These results may help us to understand the adiponectin paradox in HF.
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PMID:Nutrients restriction upregulates adiponectin in epicardial or subcutaneous adipose tissue: impact in de novo heart failure patients. 2955 29

Fibroblast growth factor (FGF) 21, a unique, largely liver-derived endocrine member of the FGF superfamily, is often thought of as a fasting factor owing to its induction in rodents during starvation. However, FGF21 is not increased by fasting for periods of <7 days in humans; instead, it rises sharply after acute alcohol and sugar intake and also after several days of overfeeding, suggesting another role in states of positive energy balance. Recent studies suggest that in the postingestive state, FGF21 may regulate energy intake and discourage consumption of alcohol and sugars, most likely through effector circuits in the central nervous system. FGF21 also increases fat oxidation in the liver, improves markers of insulin sensitivity, and stimulates adiponectin production. Thus, in primates, FGF21 may defend against hepatic nutrient overload by promoting adaptations that reduce ectopic lipid storage, including inhibiting sugar and alcohol appetite and promoting lipid sequestration in adipose tissue.
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PMID:Parsing the Potential Neuroendocrine Actions of FGF21 in Primates. 2960 70

Altay is a typical fat-tailed sheep breed displaying the unique ability to rapidly mobilize fat, which is vital for maintaining a normal metabolism that facilitates its survival in lengthy winter conditions. However, the physiological, biochemical, and molecular mechanisms underlying fat mobilization remain to be elucidated. In this study, the monitoring of rump fat adipocyte sizes disclosed a positive correlation between cell size and fat deposition ability. In addition, we subjected sheep to persistent starvation to imitate the conditions that trigger rump fat mobilization and screened 112 differentially expressed proteins using the isobaric peptide labeling approach. Notably, increased secretion of leptin and adiponectin activated the key fat mobilization signaling pathways under persistent starvation conditions. Furthermore, the upregulation of resistin (RETN), heat-shock protein 72 (HSP72), and complement factor D (CFD) promoted lipolysis, whereas the downregulation of cell death-inducing DFFA-like effector C (CIDEC) inhibited lipid droplet fusion, and the increase in HSP72 and apolipoprotein AI (Apo-AI) levels activated the body's stress mechanisms. The synergistic actions of the above hormones, genes, and signaling pathways form a molecular network that functions in improving the adaptability of Altay sheep to extreme environments. Our findings provide a reference for elucidating the complex molecular mechanisms underlying rump fat mobilization.
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PMID:Comparative Proteome Analysis Reveals Lipid Metabolism-Related Protein Networks in Response to Rump Fat Mobilization. 3015 94


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