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Acute pancreatitis (AP) entails pancreatic inflammation, tissue damage and dysregulated enzyme secretion, including pancreatic lipase (PL). The role of irisin, an anti-inflammatory and anti-apoptotic cytokine, in AP and exocrine pancreatic stress is unclear. We have previously shown that irisin regulates PL through the PPARγ-PGC1α-FNDC5 pathway. In this study, we investigated irisin and irisin's pathway on AP in in vitro (AR42J-B13) and ex vivo (rat primary acinar) models using molecular, biochemical and immunohistochemistry methodology. Pancreatitis induction (cerulein (cer)) resulted in a significant up-regulation of the PPARγ-PGC1α-FNDC5 axis, PL expression and secretion and endoplasmic reticulum (ER) stress unfolded protein response (UPR) signal-transduction markers (CHOP, XBP-1 and ATF6). Irisin addition in the cer-pancreatitis state resulted in a significant down-regulation of the PPARγ-PGC1α-FNDC5 axis, PPARγ nucleus-translocation and inflammatory state (TNFα and IL-6) in parallel to diminished PL expression and secretion (in vitro and ex vivo models). Irisin addition up-regulated the expression of pro-survival UPR markers (ATF6 and XBP-1) and reduced UPR pro-apoptotic markers (CHOP) under cer-pancreatitis and induced ER stress (tunicamycin), consequently increasing cells viability. Irisin's pro-survival effect under cer-pancreatitis state was abolished under PPARγ inhibition. Our findings suggest irisin as a potential therapeutic option for AP via its ability to up-regulate pro-survival UPR signals and activate the PPARγ-PGC1α-FNDC5 pathway. [ABSTRACT FROM AUTHOR]

The global rise in obesity is attributed to genetic predisposition interaction with an obesogenic environment. Melanocortin 4 receptor (MC4R) rs17782313 polymorphism has been linked to common obesity with varying influence across different populations. MC4R is a crucial player in the leptin proopiomelanocortin pathway that regulates weight hemostasis. We aimed to study MC4R rs17782313 and its interaction with eating behaviors on obesity predisposition in the Israeli population. Adults' (n = 5785, >18 y) genotype and anthropometric and demographic data were analyzed using logistic regression models adjusting for age, sex, T1DM, and T2DM. MC4R rs17782313 significantly predisposes to elevated obesity risk under the recessive and additive models (OR = 1.38, 95% CI: 1.1–1.72, p = 0.005 and OR = 1.1, 95% CI: 1.01–1.2, p = 0.03, respectively) adjusted for confounders (age, sex, T1DM, and T2DM). Stratification by sex demonstrated that carrying the common MC4R rs17782313 is significantly associated with an elevated predisposition to obesity under the recessive model among females only (OR = 1.41, 95% CI: 1.09–1.82, p = 0.01), with an average of 0.85 BMI increment compared with wild type and one risk allele carriers. MC4R rs17782313 significantly interacted with several eating behaviors to enhance the risk of obesity. Our findings demonstrate that MC4R rs17782313 homozygous female carriers are significantly predisposed to obesity amplified by eating behaviors. [ABSTRACT FROM AUTHOR]

Small for gestational age (SGA) is typically defined as birth weight < 10th percentile for age. Limited data are available regarding the growth of SGA preterm infants in relation to feeding type. We aimed to study SGA preterm infants fed fortified mother's own milk (MOM) or preterm formula (PF) on growth patterns and catch-up growth at discharge and 2-year corrected age (CA). Our retrospective cohort study included data from medical records and follow-up questionnaires about SGA preterm infants born at < 37 weeks fed on MOM (n 40) and PF (n 40). Weight, length/height and head circumference (HC) were collected at birth, discharge and at 2-year CA, and Δ z-scores were calculated. The MOM group had significantly larger negative change in weight and length z-scores between birth and discharge, and smaller positive change in HC z-score (–0·47 (sd 0·41) v. −0·25 (sd 0·36), P = 0·01; −0·63 (sd 0·75) v. −0·27 (sd 0·75), P = 0·03; 0·13 (sd 0·67) v. 0·41 (sd 0·55), P = 0·04, respectively). Almost half of the MOM-fed infants experienced poor length growth by discharge compared with 22 % of PF-fed infants (P = 0·03). By 2-year CA, both groups had similar positive change in weight and HC z-scores, but MOM-fed infants had a slower increase in height z-score (0·64 (sd 1·30) v. 1·33 (sd 1·33), P = 0·02), and only 40 % had achieved catch-up height compared with 68 % of the PF group (P = 0·02). Our study indicates that fortified MOM-fed SGA preterm infants may need extra nutritional support in the first 2 years of life to achieve height growth potential. [ABSTRACT FROM AUTHOR]

Sustaining adequate nutritional needs of a population is a challenging task in normal times and a priority in times of crisis. There is no 'one-size-fits-all' solution that addresses nutrition. In relevance to the COVID-19 (coronavirus disease 2019) pandemic crisis, viral infections in general and RNA viruses in particular are known to induce and promote oxidative stress, consequently increasing the body's demand for micronutrients, especially those related to antioxidant enzymic systems, thus draining the body of micronutrients, and so hindering the human body's ability to cope optimally with oxidative stress. Common polymorphisms in major antioxidant enzymes, with world population minor allele frequencies ranging from 0·5 to 50 %, are related to altered enzymic function, with substantial potential effects on the body's ability to cope with viral infection-induced oxidative stress. In this review we highlight common SNP of the major antioxidant enzymes relevant to nutritional components in the context of viral infections, namely: superoxide dismutases, glutathione peroxidases and catalase. We delineate functional polymorphisms in several human antioxidant enzymes that require, especially during a viral crisis, adequate and potentially additional nutritional support to cope with the pathological consequences of disease. Thus, in face of the COVID-19 pandemic, nutrition should be tightly monitored and possibly supplemented, with special attention to those carrying common polymorphisms in antioxidant enzymes. [ABSTRACT FROM AUTHOR]