The developmental changes of both pancreatic and intestinal enzymes and the influence of dietary composition on enzyme activities were followed in suckling and weaning rabbits. In addition, whole tract digestibility of nutrients was recorded in response to two dietary energetic sources. Rabbits were fed ad libitum either a low fat and high starch diet (group LF), or a high fat and high fibre diet (group HF) between d 32 and d 42, with both groups receiving a growing finishing diet thereafter. Before weaning (d 32) nutrient digestion was high (>75% for organic matter, protein or fat), and then decreased sharply, except for fat. Between d 32 and d 42, digestion in the HF group was 7.5 and 4.6% lower, respectively, for organic matter and protein, while fibre and fat digestion was higher (+14.0 and +5.0%, respectively). Between d 25 and d 42 of age, pancreatic-specific activities of trypsin and chymotrypsin did not change while those of amylase and lipase increased by 1.5- and 76- fold (P<0.05), respectively. However, total activities and relative activities expressed on a LW basis were increased after weaning as a main consequence of a specific increased organ weight and pancreatic protein content. Relative activities of trypsin and chymotrypsin increased by 63 and 56% (P<0.01) after weaning, respectively. Total activities of pancreatic enzymes measured in the total small intestinal contents increased during the same period, but the range of variations was lower than those measured in the pancreatic gland. Total activities of lipase, trypsin and chymotrypsin measured in the small intestine contents were significantly correlated with pancreas enzyme potentialities. Total small intestine activity of lipase was 58% higher (P<0.001) in HF than in LF group while the other pancreatic and intestinal enzyme activities measured were not influenced by the energetic sources of the diet. Decreased digestibility of organic matter and protein observed with the HF diet could not be related to changes in pancreatic or intestinal enzymatic profiles and may be more dependent on quality of dietary ingredients.
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http://dx.doi.org/10.1016/s1095-6433(03)00112-0 | DOI Listing |
J Anim Ecol
January 2025
Department of Marine Science, Marine Science Institute, The University of Texas at Austin, Port Aransas, Texas, USA.
Marine heatwaves are increasingly common due to human-induced climate change. Under prolonged thermal stress on coral reefs, corals can undergo bleaching, leading to mass coral mortality and large-scale changes in benthic community composition. While coral mortality has clear, negative impacts on the body condition and populations of coral-dependent fish species, the mechanisms that drive these changes remain poorly resolved.
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Department of Anthropology, Baylor University, Waco, Texas, USA.
Oxidative stress (OS) is a key biological challenge and selective pressure for organisms with aerobic metabolism. The result of the imbalance between reactive oxygen species production and antioxidant defense, OS can damage proteins, lipids, and nucleic acids and plays an important role in driving variation in biological aging and health. Among humans, OS research has focused overwhelmingly on adults, with demonstrated connections between OS, inflammation, and metabolic and neurodegenerative conditions.
View Article and Find Full Text PDFMol Metab
January 2025
Institut Numecan, INRAE, INSERM, Univ Rennes, Rennes, France. Electronic address:
Objective: Obesity and overweight are associated with low-grade inflammation induced by adipose tissue expansion and perpetuated by altered intestinal homeostasis, including increased epithelial permeability. Intestinal epithelium functions are supported by intestinal epithelial cells (IEC) mitochondria function. However, diet-induced obesity (DIO) may impair mitochondrial activity of IEC and consequently, intestinal homeostasis.
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The Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Bethesda, Maryland, USA.
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View Article and Find Full Text PDFVet Sci
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CONAHCYT-UAM Xochimilco, Universidad Autónoma Metropolitana Xochimilco, Mexico City 04960, Mexico.
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