👤 Maria E Secci

This study investigated the hepatic expression of genes involved in stress response (CASP6, CAT, SOD1, HSPA2) and lipid metabolism (LPL, SREBF, FABP1, ACOX1, FADS2) in a local slow-growing chicken breed, the Bionda Piemontese (BP), following two isonitrogenous diets (crude protein, 170 g/kg as fed): a control diet (L) and a high-fat diet (H) obtained by supplementing 6 % palm kernel oil, during the finisher period. Sixty (male and female) chickens were included in the study and slaughtered at five months of age. RNA was extracted from 36 liver samples (18 male and 18 female) and sequenced using the targeted RNA-seq method followed by bioinformatic analysis using DESeq2 to detect differences in gene expression. Overall, the high-fat dietary supplementation did not significantly alter the expression of most stress-related genes, indicating that the high-fat diet did not elicit a hepatic stress response in BP chickens. However, within each sex, the high-fat diet tended to upregulate FADS2 and FABP1 in females, and slightly downregulate ACOX1 in males. Considering sex as an independent factor, FABP1 expression was higher in females, whereas males exhibited significantly higher LPL expression. These findings highlight a clear sexual dimorphism in hepatic lipid gene expression in BP chickens. While dietary fat supplementation had limited impact on differentially expressed genes, the study underscores the importance of sex in shaping metabolic gene expression. It also provides evidence supporting the possible metabolic resilience of the BP breed to tolerate changes in dietary fat content. Further studies are needed to substantiate this claim, and to investigate the long-term effects and the tissue-specific responses of dietary fat supplementation in other organs. Show less

Chronic inflammatory pain represents one of the largest subsets of chronic pain diagnoses, which affect nearly a quarter of individuals in the United States and cost nearly $600 billion dollars annually. Chronic pain leads to persistent sensory hypersensitivities, as well as emotional and cognitive disturbances. Evidence suggests that melanocortin 4 receptors (MC4Rs) mediate pain-signaling and pain-like behaviors via actions at various nodes in the pain-neural axis, but the field lacks a complete understanding of the potential role of MC4Rs in chronic inflammatory pain in males and females. The central amygdala (CeA) expresses high quantities of MC4R and receives pain-related information from the periphery, and in vivo CeA manipulations alter nociceptive behavior in pain-naïve and in animals with chronic pain. Here, we tested the hypothesis that MC4Rs in the CeA modulate thermal nociception and mechanical sensitivity, as well as pain avoidance, in male and female Wistar rats, using a model of chronic inflammatory pain (Complete Freud's Adjuvant; CFA). First, we report that CFA produces long-lasting hyperalgesia in adult male and female Wistar rats, and long-lasting pain avoidance in male Wistar rats. Second, we report that MC4R antagonism in the CeA reduces thermal nociception and mechanical sensitivity in male and female Wistar rats treated with CFA. Finally, we report that MC4R antagonism in the CeA reduces pain avoidance in male, and that this effect is not due to drug effects on locomotor activity. Our results indicate that a model of chronic inflammatory pain produces long-lasting increases in pain-like behaviors in adult male and female Wistar rats, and that antagonism of MC4Rs in the CeA reverses those effects. Show less