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Different functional responsibility of the small intestine to high-fat/high-energy diet determined the expression of obesity-prone and obesity-resistant phenotypes in rats
Zuzana Šefčíková, Tomáš Hájek, Ľudovít Lenhardt, Ľubomír Raček, Štefan Mozeš
Jazyk angličtina Země Česko
NLK
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- MeSH
- adipozita MeSH
- alkalická fosfatasa metabolismus MeSH
- časové faktory MeSH
- dietní tuky MeSH
- energetický metabolismus MeSH
- energetický příjem MeSH
- fenotyp MeSH
- financování organizované MeSH
- fyziologická adaptace MeSH
- glukosidasy metabolismus MeSH
- hmotnostní přírůstek MeSH
- homeostáza MeSH
- hypertrofie MeSH
- krysa rodu rattus MeSH
- modely nemocí na zvířatech MeSH
- náchylnost k nemoci MeSH
- obezita MeSH
- potkani Sprague-Dawley MeSH
- přijímání potravy MeSH
- střevní sliznice metabolismus MeSH
- tenké střevo MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
The objective of the present experiment was to assess the involvement of small intestine in expression of susceptibility or resistance to the high-fat/high-energy diet. The investigation was carried out in adult male Sprague-Dawley rats fed either standard laboratory diet (3.2 kcal/g, 9.5 % fat) or high-fat (HF) diet (4.04 kcal/g, 30 % fat) for 4 weeks as well as in HF rats that were retrospectively designated on the bases of their higher or lower weight gain as sensitive (DIO) or resistant (DR) to obesity. Our results revealed in HF group significant increase in energy intake, food efficiency, weight gain and Lee s index of obesity. Moreover, in comparison with controls, a significantly increased duodenal and jejunal alkaline phosphatase (AP) and alpha-glucosidase activity as well as hypertrophy of jejunal mucosa (increased protein/DNA ratio) were observed in HF fed rats. In contrast, intestinal function was inversely related to energy intake or to the development of adiposity in DIO vs. DR rats. The DR rats had significantly greater AP and alpha-glucosidase activity and more pronounced suppression of energy intake than obese DIO rats. It indicates that the increase of enzyme activities and the lowered effectiveness of nutrient absorption might be a significant factor preventing the expression of obesity proneness. This information contributes to a better understanding of a complex interaction between HF diet feeding and small intestinal adaptability, which determines the energy homeostasis and predict the ability to resist or develop obesity in these phenotypes.
Citace poskytuje Crossref.org
Lit.: 31
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- $a The objective of the present experiment was to assess the involvement of small intestine in expression of susceptibility or resistance to the high-fat/high-energy diet. The investigation was carried out in adult male Sprague-Dawley rats fed either standard laboratory diet (3.2 kcal/g, 9.5 % fat) or high-fat (HF) diet (4.04 kcal/g, 30 % fat) for 4 weeks as well as in HF rats that were retrospectively designated on the bases of their higher or lower weight gain as sensitive (DIO) or resistant (DR) to obesity. Our results revealed in HF group significant increase in energy intake, food efficiency, weight gain and Lee s index of obesity. Moreover, in comparison with controls, a significantly increased duodenal and jejunal alkaline phosphatase (AP) and alpha-glucosidase activity as well as hypertrophy of jejunal mucosa (increased protein/DNA ratio) were observed in HF fed rats. In contrast, intestinal function was inversely related to energy intake or to the development of adiposity in DIO vs. DR rats. The DR rats had significantly greater AP and alpha-glucosidase activity and more pronounced suppression of energy intake than obese DIO rats. It indicates that the increase of enzyme activities and the lowered effectiveness of nutrient absorption might be a significant factor preventing the expression of obesity proneness. This information contributes to a better understanding of a complex interaction between HF diet feeding and small intestinal adaptability, which determines the energy homeostasis and predict the ability to resist or develop obesity in these phenotypes.
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