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547.918 --- 641.883 --- 641.13 --- Academic collection --- Glycosides. Amygdalin. Hesperidin. Saponin. Digitalin. Coniferin. Stevioside --- Sweeteners. Sugar --- Carbohydrates. Cereals. Fruits. Sugars --- Conferences - Meetings --- 641.13 Carbohydrates. Cereals. Fruits. Sugars --- 641.883 Sweeteners. Sugar --- 547.918 Glycosides. Amygdalin. Hesperidin. Saponin. Digitalin. Coniferin. Stevioside
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Biodiversiteit --- Biodiversity --- Biodiversité --- Biological diversification --- Biological diversity --- Biological products --- Biologische producten --- Biologische verscheidenheid --- Bioproducten --- Bioproducts --- Biotic diversity --- Diversification [Biological ] --- Diversity [Biological ] --- Diversity [Biotic ] --- Diversité biologique --- Producten [Biologische ] --- Products [Biological ] --- Produits biologiques --- # BIBC : Academic collection --- 573.9 --- biodiversiteit (lt) --- ecosysteem (lt) --- dierproductiesystemen (lt) --- 574.1 --- Landbouw --- Biotechnologie --- Voedingsleer --- Suiker --- Voedingsingredienten --- Vetten --- Olie (plantaardige) --- Biobrandstoffen --- Biodiversiteit (bedreigde diersoorten, bedreigde planten) --- 57.08 --- biodiversiteit --- Biological techniques. Experimental methods. Equipment --- 57.08 Biological techniques. Experimental methods. Equipment --- PXL-Tech 2015 --- opleiding biotechnologie --- milieuzorg --- bio-productietechnologie
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AMPK is a heterotrimeric enzyme, which plays an important role in cellular energy balance in eukaryote species. Mammalian studies suggested that AMPK pathways in the central and peripheral tissues coordinately integrates inputs from multiple sources to regulate energy balance at a whole-body level. In this dissertation, we explored the potential role of AMPK in the regulation of energy homeostasis in broiler chickens.During incubation, there is an inevitable spread of hatching time for late versus early hatching chicks. We found that female chicks hatched at a different time exhibited distinct neonatal performance: the feed intake and growth rate of the late hatchers were higher as compared to that of the early hatchers. The late hatchers had higher glycogen contents in the liver and the hatching muscle, and utilized yolk more rapidly compared to their early counterparts. Thereby, we investigated the involvement of hypothalamic and hepatic AMPK and potential effectors in the spread of hatching time model. As a result, hypothalamic AMPKα1 isoform gene expression was significantly higher in the late hatcher as compared to that of their early counterparts. The hypothalamic orexigenic NPY and AgRP mRNA levels were higher in the late hatchers as compared to the early. In the liver, AMPKα2 mRNA level and the phosphorylation ratio of AMPKα was significantly lower in the late hatchers, as compared to their early counterparts. The hepatic phosphorylated GS levels of the late and middle hatchers were lower than that of their early counterparts. Taken together, AMPK may play a significant role in the different neonatal performance of the spread of hatching time model. The central and peripheral AMPK in late hatchers exhibited a pattern of higher energy intake and lower energy expenditure, which resulted in a faster post-hatch growth.In order to specifically target AMPK, a mammalian central AMPK inhibitor, α-LA, was supplemented to the diet of broiler chicks for seven days, and hypothalamic and hepatic AMPK and downstream targets were monitored. As a result, dietary α-LA decreased feed intake of broiler chicks independent of the taste aversion. The anorectic effect was due to the reduced hypothalamic phosphorylated AMPKα as reflected in its decreased mRNA and protein levels. However, the anorectic effect of α-LA was progressively diminished after 7 days of treatment, likely by a physiological counteractive feedback via changing neuropeptides involved in energy balance regulation. In liver, on the other hand, α-LA decreased the hepatic glycogenesis and lipogenesis via stimulating hepatic AMPKα in mRNA levels and phosphorylation. The stimulatory effect of α-LA on hepatic AMPK together with the inhibitory effect on hypothalamic AMPK may have altered the energy balance and hence impaired body weight gain of broiler chicks.Recent years, there is a growing interest in studying the role of dietary protein in energy regulation using isocaloric low protein diets. Here we investigated the response of hypothalamic AMPK and (an)orexigenic neuropeptides to this diet providing lower crude protein yet sufficient energy in broiler chicks. As a result, broiler chicks fed with isocaloric low protein diet attained higher feed intake likely through decreasing hypothalamic anorexigenic POMC and SREBP-1 as an attempt to meet the protein needs. Plasma thyroid hormones and corticosterone results indicated an increment in energy expenditure resulting in a decreased growth rate of those protein malnutrition chicks. The decreased AMPKα activity suggested that AMPK is prone to be changed by the overall energy intake, but not ingested protein alone, to regulate energy balance.In conclusion, AMPK is involved in the regulation of feed intake and energy homeostasis in chickens. However, the changes of hypothalamic AMPK, expression and/or activity, are not always consistent with the (an)norexigenic neuropeptides, indicating that the regulatory mechanism of AMPK on hypothalamic (an)orexigenic neuropeptides are indirect and not necessary. AMPK may play a role in the regulation of carbohydrate and lipid metabolisms in chickens as in mammals. Moreover, the response of chicken AMPK to the changes of energy status is tissue-specific.
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