BACKGROUND: Malnutrition is associated with clinical factors, including longer hospital stay, increased morbidity and mortality and hospital costs. OBJECTIVE: To investigate the prevalence of malnutrition using different nutritional indicators and to identify factors that contribute to malnutrition in hospitalized patients. METHODS: We investigated anthropometric, laboratory standards, nutritional risk screening (NRS), subjective global assessment (SGA), mini nutritional assessment and habitual energy consumption (HEC). Chi-square, Fisher’s exact test, Mann-Whitney test and univariate and multiple Cox regression analysis were used, at 5% significance level. RESULTS: It was found 21.01% of malnourished individuals by ASG; a total of 34.78% with nutritional risk according to NRS and 11.59% with low weight (BMI). There was no statistically significant difference in the prevalence of malnutrition by ASG (P=0.3344) and nutritional risk by NRS (P=0.2286), among the types of disorders. Patients with nutritional risk were of higher median age (64.5 vs 58.0 years; P=0.0246) and had lower median values of HEC (1362.1 kcal vs 1525 kcal, P=0.0030), of calf circumference (32.0 cm vs 33.5 cm, P=0.0405) of lymphocyte count (1176.5 cell/mm3 vs 1760.5 cell/ mm3, P=0.0095); and higher percentage of low body weight according to the BMI (22.9% vs 5.6%; P=0.0096). Lymphocyte count was associated with nutritional risk (P=0.0414; HR= 1.000; IC95%= 0.999; 1.000). CONCLUSION: NRS was more sensitive than other indicators in the diagnosis of malnutrition. Patients at risk were older and had lower HEC values, calf circumference, BMI and lymphocyte count. Low lymphocyte count was considered a factor associated with nutritional risk by the NRS.

Recent studies demonstrate that α7 nicotinic acetylcholine receptors (α7nAChR) in hypothalamic neurons, including pro-opiomelanocortin (POMC) neurons, modulate energy homeostasis. This study aimed to explore how the α7nAChR subunit in hypothalamic POMC neurons affects food intake and energy balance in mice. This study used site-specific knockout mice for α7nAChR in POMC neurons (Control: α7nAChR^fl/fl; Knockout: α7nAChR^fl/flPOMC^Cre) generated via the Cre-LoxP system. Body weight (BW) and body weight gain (BWG) were measured. We measured energy expenditure by respirometry and assessed glycemic homeostasis using an intraperitoneal glucose tolerance test (ipGTT) and an insulin tolerance test (ipITT). Food intake was measured after intraperitoneal injection of saline (0.9%), leptin (5 μg/g BW), or the selective α7nAChR agonist PNU-282987 (1 mg/kg BW). Afterward, fasted mice were injected intraperitoneally with saline (0.9%), leptin (2.5 μg/g BW), or PNU-282987 (1 mg/kg BW), and subsequently euthanized. RT-qPCR and Western blotting analyses were performed. The α7nAChR^fl/flPOMC^Cre males were initially lighter but had higher BWG. The opposite was observed in females. α7nAChR^fl/flPOMC^Cre male mice showed increased epididymal fat, serum leptin levels, and food intake. Knockout male mice showed no major impairment in glucose homeostasis and signaling. Furthermore, the leptin-induced anorectic response was delayed, with reduced hypothalamic anorectic proteins and a trend toward reduced pCREB^Ser133 after an acute leptin stimulus. PNU-282987 treatment increased pCREB^Ser133 content and Pcsk1 gene expression in vitro. The α7nAChR expressed in POMC neurons seems to contribute to energy and glycemic homeostasis and to the hypothalamic leptin-induced anorectic response mediated by CREB phosphorylation.