Abstract
Adenosine monophosphate-activated protein kinase (AMPK) acts as a sensor of cellular energy changes and is involved in the control of food intake. A total of 216 1-d-old broilers were randomly allotted into 3 treatments with 6 replicates per treatment and 12 broilers in each cage. The dietary treatments included 1) high-energy (HE) diet (3,500 kcal/kg), 2) normal-energy (NE) diet (3,200 kcal/kg), and 3) low-energy (LE) diet (2,900 kcal/kg). The present study was conducted to investigate the effects of dietary energy level on appetite and the central AMPK signal pathway. The results showed that a HE diet increased average daily gain (ADG), whereas a LE diet had the opposite effect (P < 0.05, N = 6). The average daily feed intake (ADFI) of the chickens fed the LE diet was significantly higher than that of the control (P < 0.05, N = 6). Overall, the feed conversion rate gradually decreased with increasing dietary energy level (P < 0.05, N = 6). Moreover, the chickens fed the LE and HE diets demonstrated markedly improved urea content compared with the control group (P < 0.0001, N = 8). The triglyceride (TG) content in the LE group was obviously higher than that in the HE group but showed no change compared with the control (P = 0.0678, N = 8). The abdominal fat rate gradually increased with increased dietary energy level (P = 0.0927, N = 8). The HE group showed downregulated gene expression levels of liver kinase B1 (LKB1), neuropeptide Y (NPY), cholecystokinin (CCK), and glucocorticoid receptor (GR) in the hypothalamus compared with the control group (P < 0.05, N = 8). However, LE treatment significantly increased the mRNA level of AMP-activated protein kinase α2 (AMPKα2) compared with other groups (P = 0.0110, N = 8). In conclusion, a HE diet inhibited appetite and central AMPK signaling. In contrast, a LE diet activated central AMPK and appetite. Overall, the central AMPK signal pathway and appetite were modulated in accordance with the energy level in the diet to regulate nutritional status and maintain energy homeostasis in birds.
Highlights
The regulation of voluntary food intake in animals and humans is complex and involves central and peripheral regulatory mechanisms (Lenard and Berthoud, 2008)
Feed intake increased with decreased nutrient density, supporting the prevailing viewpoint that feed intake (FI) in broilers is regulated on the basis of nutrient density (Nielsen, 2004)
Yuan et al (2008) found that high energy diet (HED) chickens had significantly higher plasma insulin levels and that dietary energy levels were associated with impaired glucose-insulin balance
Summary
The regulation of voluntary food intake in animals and humans is complex and involves central and peripheral regulatory mechanisms (Lenard and Berthoud, 2008). In the central nervous system (CNS), the hypothalamus is the brain region that regulates food intake and energy homeostasis (Gustavo et al, 2013), and the arcuate nucleus (ARC) of the hypothalamus is believed to play a crucial role in these processes (Sam et al, 2012). Hypothalamic 5′-adenosine monophosphate-activated protein kinase (AMPK), composed of α, β, and γ subunits (Hardie et al, 2012), senses intracellular metabolic stress, increases the cellular AMP:ATP ratio, and integrates diverse hormonal and nutritional signals to maintain energy balance (Gustavo et al, 2013). Increasing evidence has shown that AMPK has a central role in mediating the appetite-modulating and metabolic effects of several hormones and substances (Kola et al, 2006). High-fat diet-induced obesity can alter AMPK activity in the hypothalamus and skeletal muscle (Martin et al, 2006)
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