Higher THI indices recorded during the summer season compared to those recorded during the autumn season reveal that the birds are exposed to heat stress during the summer (Fig 1;
Jayasri et al., 2022b). The stress ranges for poultry have been reported previously based on THI: <27.8 as normal, 27.8-28.8 as moderate, 28.9-29.9 as severe and ≥30.0 as very severe
(Lallo et al., 2018).
An increase (
P<0.01) in serum triglyceride, total cholesterol and LDL levels was observed during the summer compared to autumn (Table 3), which is in agreement with earlier reports
(Xie et al., 2015). Hyperlipidemia observed during summer was associated with elevated cortisol levels in the present study (Table 4). The role of corticosteroids in hyperlipidemia during stress was reported earlier, where it was found to increase the triglycerides, total cholesterol, HDL and LDL fractions of cholesterol in serum during HS in broilers
(Pulai et al., 1997; Eid et al., 2003). Stress-induced depression in insulin secretion might enhance the activity of lipolytic enzymes and be responsible for increased serum lipids
(Ognik and Sembratowicz, 2012). A significant (
P<0.05) increase in blood glucose levels (23% at 42 d) observed during summer (Table 4), is consistent with the previous findings (
Ognik and Sembratowicz, 2012;
Bai et al., 2019). Enhanced cellular energy demand during stress drives glucose output from the liver, resulting in increased blood glucose levels. Insulin resistance reported during HS could lead to a decrease in the utilization of glucose, further contributing to hyperglycemia
(Hargreaves et al., 1996; Honda et al., 2007).
Selenium supplementation resulted in a significant (
P<0.01) reduction of serum TG levels at 21 d. SeMet at 0.3 ppm was found to be effective in reducing serum TC and LDL levels at 21 d, while 0.6 ppm was effective at 42 d (Table 3). The hypolipidemic effect of selenium at low doses on serum cholesterol was reported earlier in rats with induced hyperlipidemia (
Sreekala and Indira, 2008;
Zhang et al., 2018). SeMet supplementation at 0.9 ppm was found to increase serum TC and LDL levels. Similar to the present findings, an increase in plasma TC has been reported in chickens fed with supranutritional Se (3 ppm) under thermoneutral conditions
(Huang et al., 2016). The association of high plasma selenium levels with hyperglycemia and hyperlipidemia was also revealed by the epidemiological data in humans
(Steinbrenner et al., 2011).
Serum glucose concentration increased further with SeMet supplementation beyond 0.3 ppm at 21 d, whereas 0.6 ppm showed a hypoglycemic effect at 42 d when compared to the summer control (Table 4). Selenium is reported to influence glucose metabolism by improving insulin secretion and signaling
(Fontenelle et al., 2018). However, Se in excess of the required amount has been shown to inhibit growth in chickens by increasing blood glucose levels
(Xiang et al., 2017). The hyperglycemia observed with a higher selenium dose in the present study is supported by earlier reports of higher dietary selenium-induced hyperinsulinemia and insulin resistance resulting in hyperglycemia in different animal models like rats, pigs and chicken
(Xu et al., 2017). The findings of the present study showed that higher blood glucose levels observed at 0.9 ppm SeMet were associated with poor growth performance (Table S1).
Serum cortisol and T
4 levels were significantly (P<0.05) increased while T3 levels decreased at 42 d during summer (Table 4), which is in agreement with previous reports
(Sohail et al., 2010, Rajaei
Sharifabadi et al., 2017). Selenium supplementation showed a dose-dependent effect on cortisol levels, whereas it showed a plateau effect on serum T
3 levels at 42 days. Similar to the present findings, the ameliorative effect of 0.4 ppm selenium was reported earlier against the effect of oxidative stress on serum thyroxine levels in broilers
(Fan et al., 2009).
The liver is the primary organ of lipogenesis and is responsive to HS in poultry
(Flees et al., 2017). Several studies have reported that HS can enhance fat synthesis and deposition in broilers despite a substantial reduction in feed intake
(Geraert et al., 1996b; Lu et al., 2007). The relative change observed in the expression of ACCa and FASN mRNA at 21 d was 4.90 and 2.25 fold, while it was 0.36 and 0.35 fold, respectively, at 42 d during summer when compared to autumn (Table 5). The enhanced expression of ACCa and FASN at 21 d is in agreement with previous findings where ACC expression in the liver was up-regulated during HS (8 hr./d for one week) in broilers
(Jastrebski et al., 2017). However, such studies were conducted for a brief period of time,
i.e., acute heat stress.
The decreased expression of ACCα and FASN mRNA at 42 d of summer is in concurrence with previous reports indicating adaptive responses of broilers to high temperatures
(Flees et al., 2017; Lu et al., 2019). The reduced fatty acid synthesis at 42 d was associated with negative energy balance, as shown by poor feed consumption and an increase in the antioxidant activity and expression of PGC-1 in liver tissue
(Jayasri et al., 2022a). Hepatic lipogenesis is highly responsive to changes in the diet, the energy status of the cell and the subsequent responses of key plasma metabolic hormones in broilers
(Huang et al., 2008). Negative energy balance during HS (due to reduced feed intake and increased functioning of antioxidant machinery) could result in reduced serum glucagon levels, further contributing to a decrease in lipogenesis during chronic stress
(Flees et al., 2017; Rix et al., 2019).
Prolonged heat stress along with the increased activity of antioxidant enzymes could result in impaired insulin signaling
(Huang et al., 2018), which is further responsible for decreased expression of
de novo lipogenic genes. Despite the decrease in lipogenesis, serum TG, TC and LDL concentrations increased at 42 d, which could be due to the release of intracellular storage lipids rather than
de novo synthesis. This might be essential to meet the energy deficit created during summer, as evidenced by the elevated levels of PGC-1
(Jayasri et al., 2022a).
Selenium supplementation resulted in a decrease in the expression of ACCα and FASN both at 21 d and 42 d during the summer. A similar trend was reported earlier, where a significant reduction in abdominal fat content was observed upon selenium supplementation at 0.33 ppm in quails during HS (
Del Vesco et al., 2017). The results of the present study are in agreement with a previous report where the suppression of hepatic
de novo fatty acid synthesis due to dietary supplementation with Se and Mg at both high and low doses in high-fat-fed rats was observed
(Zhang et al., 2018). Long-term selenium supplementation has also been shown to reduce hepatic steatosis in mice by reducing the mRNA levels of the ACC1 and FASN genes
(Miyata et al., 2020). The role of selenoprotein P in reducing the activity of ACC was reported earlier in mouse hepatic tissues
(Misu et al., 2010). Thus, the suppressive effect of selenium on
de novo lipid metabolism during summer may be due to its effect on the cellular redox state, which is known to influence insulin secretion and signaling
(Fontenelle et al., 2018).
