Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020505 (hyperphagia)
6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The novel satiety factor nesfatin-1 has been shown to decrease food intake and body weight in rodents after i.c.v. injection. However, no further developments regarding the true patho-physiological relevance of nesfatin-1 in obesity and type 1 diabetes mellitus (T1 DM) and type 2 diabetes mellitus (T2 DM) have been reported. A recent study by Stengel et al. demonstrated that a down-regulation of NUCB2 mRNA in gastric endocrine cells was observed after 24-h fasting. They raised the possibility that nesfatin/NUCB2 gene expression may be regulated by nutritional status, suggesting that nesfatin-1 in the stomach might play a role in satiety. In the present study, fasting levels in plasma nesfatin-1, insulin and glucose were measured and analyzed in healthy subjects and in patients with T1 DM and T2 DM. Plasma nesfatin-1 levels were measured 6 times before and after oral glucose ingestion in healthy subjects. No sex differences in plasma nesfatin-1 were found. The mean fasting plasma nesfatin-1 levels were slightly but not significantly higher in T1 DM patients compared to healthy subjects. However, fasting plasma nesfatin-1 levels were significantly lower in T2 DM patients compared to healthy subjects and T1 DM patients. Plasma nesfatin-1 did not change acutely, although a small rise in circulating nesfatin-1 occurred within 30 min after the beginning of an oral glucose ingestion (from a mean basal value of 0.99+/-0.23 ng/ml to a maximum of 1.08+/-0.24 ng/ml). No significant difference in plasma nesfatin-1 before and after an oral glucose was observed. In conclusion, we showed that fasting nesfatin-1 was significantly lower in T2 DM patients compared to healthy subjects and T1 DM patients. The significance of this result is unclear but the reduction in fasting nesfatin-1 may be one of the appetite-related hormones involved in diabetic hyperphagia. In addition, neither glucose nor saline ingestions affected plasma nesfatin-1, suggesting that gastric chemosensation is not sufficient for the nesfatin-1 response under the present conditions.
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PMID:Fasting plasma levels of nesfatin-1 in patients with type 1 and type 2 diabetes mellitus and the nutrient-related fluctuation of nesfatin-1 level in normal humans. 1989 82

The recently discovered nesfatin-1 is regulated by hunger and satiety. The precursor protein NUCB2 is proteolytically cleaved into three resulting fragments: nesfatin-1, nesfatin-2, and nesfatin-3. The middle segment of nesfatin-1 (M30) is responsible for limiting food intake, while the exact physiological role of nesfatin-2 and nesfatin-3 are not currently known yet. This hormone plays role/roles on diabetic hyperphagia, epilepsy, mood, stress, sleeping, anxiety, hyperpolarization, depolarization, and reproductive functions. This review will address nesfatin, focusing on its discovery and designation, biochemical structure, scientific evidence of its anorexigenic character, the results of the human and animal studies until the present day, its main biochemical and physiological effects, and its possible clinical applications.
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PMID:Multi-functional peptide hormone NUCB2/nesfatin-1. 2352 35