Chronic Mild Cold Conditioning Modulates the Expression of Hypothalamic Neuropeptide and Intermediary Metabolic-Related Genes and Improves Growth Performances in Young Chicks

Abstract

BackgroundLow environmental temperatures are among the most challenging stressors in poultry industries. Although landmark studies using acute severe cold exposure have been conducted, still the molecular mechanisms underlying cold-stress responses in birds are not completely defined. In the present study we determine the effect of chronic mild cold conditioning (CMCC) on growth performances and on the expression of key metabolic-related genes in three metabolically important tissues: brain (main site for feed intake control), liver (main site for lipogenesis) and muscle (main site for thermogenesis).Methods80 one-day old male broiler chicks were divided into two weight-matched groups and maintained in two different temperature floor pen rooms (40 birds/room). The temperature of control room was 32°C, while the cold room temperature started at 26.7°C and gradually reduced every day (1°C/day) to reach 19.7°C at the seventh day of the experiment. At day 7, growth performances were recorded (from all birds) and blood samples and tissues were collected (n = 10). The rest of birds were maintained at the same standard environmental condition for two more weeks and growth performances were measured.ResultsAlthough feed intake remained unchanged, body weight gain was significantly increased in CMCC compared to the control chicks resulting in a significant low feed conversion ratio (FCR). Circulating cholesterol and creatine kinase levels were higher in CMCC chicks compared to the control group (P<0.05). CMCC significantly decreased the expression of both the hypothalamic orexigenic neuropeptide Y (NPY) and anorexigenic cocaine and amphetamine regulated transcript (CART) in chick brain which may explain the similar feed intake between the two groups. Compared to the control condition, CMCC increased the mRNA abundance of AMPKα1/α2 and decreased mTOR gene expression (P<0.05), the master energy and nutrient sensors, respectively. It also significantly decreased the expression of fatty acid synthase (FAS) gene in chick brain compared to the control. Although their roles are still unknown in avian species, adiponectin (Adpn) and its related receptors (AdipoR1 and 2) were down regulated in the brain of CMCC compared to control chicks (P<0.05). In the liver, CMCC significantly down regulated the expression of lipogenic genes namely FAS, acetyl-CoA carboxylase alpha (ACCα) and malic enzyme (ME) and their related transcription factors sterol regulatory element binding protein 1/2 (SREBP-1 and 2). Hepatic mTOR mRNA levels and phosphorylated mTOR at Ser2448 were down regulated (P<0.05), however phosphorylated ACCαSer79 (inactivation) was up regulated (P<0.05) in CMCC compared to control chicks, indicating that CMCC switch hepatic catabolism on and inhibits hepatic lipogenesis. In the muscle however, CMCC significantly up regulated the expression of carnitine palmitoyltransferase 1 (CPT-1) gene and the mRNA and phosphorylated protein levels of mTOR compared to the control chicks, indicating that CMCC enhanced muscle fatty acid β-oxi...

Endocrinology of thermoregulation in birds in a changing climate

“…It is also well understood that many hormonal axes are likely to interact (see also above). (i) Nguyen et al (2015) discovered that hypothalamic orexigenic neuropeptide Y (NPY) responds to cold exposure in poultry. (ii) Melatonin, an indoleamine produced in the pineal gland, has been implicated to play a role in avian thermal homeostasis (John and George, 1991).…”

A Novel Mutation in the Promoter Region of Avian Uncoupling Protein3 Associated with Feed Efficiency and Body Composition Traits in Broiler Chicken.

“…Moreover, in the human field, some supportive investigations have indicated common mutations on promoter sites of UCP3 are associated with childhood obesity, energy expenditure, body weight alteration, and BMI (Mutombo et al, 2013;Brondani et al, 2014). Almost every research conducted on UCP3 recommended some promotion in feed efficiency and growth performance traits in chicken associated with UCP3 polymorphism in chicken (Nguyen et al, 2015;Moazeni et al, 2016;Jin et al, 2018), in Japanese quail (Murata et al, 2013), in New Zealand Romney lambs (An et al, 2018), and in Angus' steers (Kolath et al, 2006). Furthermore, recent studies suggest that proton uncoupling action of UCP3 in mitochondria can permit heat production and regulate energy metabolism in beige adipose tissue in pigs (Cieslak et al, 2009;Lin et al, 2017).…”

“…Whereas, regulation of UCP3 expression appeared to be related with Free Fatty Acid (FFA) utilization and free radical metabolism (Jian-Guo et al, 2005;Murata et al, 2013; DOI: https://dx.doi.org/10.36380/jwpr.2020.12 Moazeni et al, 2016). Therefore, avUCP can act as similar to mammalian UCPs, which have been strongly inducing during cold-exposure states (Raimbault et al, 2001;Masaaki et al, 2002;Rey et al, 2010;Nguyen et al, 2015;Lin et al, 2017).…”

A New Insight into Cold Stress In Poultry Production

“…Our data show that CMCC improved the growth performance of chicks during the first week post-hatch and their later lives in terms of body weight gain and Feed Conversion Ratio (FCR). 13 Plasma cholesterol and creatine kinase (CK) levels increased indicating a potential role of CK in maintaining high ATP turnover in a hypothermal condition.…”

“…CMCC also modulated the hepatic expression of lipogenic genes, which implies the inhibition of fatty acid synthesis in cold stress chicks. 13 Moreover, CMCC enhanced muscle fatty acid β-oxidation through affecting the gene and protein expression of carnitine palmitoyl transferase-1 (CPT-1) and phosphorylated mTOR. In summary, the CMCC used in our study could improve later growth performance of young chicks (body weight gain and FCR).…”