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Alterations in the mucosal processing of iron in response to very-short-term dietary iron depletion and repletion.

ABSTRACT: The transfer of control rats to a low-iron diet for only 24 h resulted in a 2-fold increase in iron uptake by brush-border membrane vesicles. Extension of the low-iron feeding period to 72 h or 2 weeks resulted in only small additional increases in iron uptake by vesicle preparations. In contrast, the transfer of iron-deficient rats to a control diet resulted in a progressive decrease in iron uptake by vesicles that reached a level equivalent to that of control rats in 2 weeks. 59Fe labelling of detergent extracts of these vesicle preparations provided evidence for the presence of an iron-binding protein composed of subunits of 52,000 Da. The changes in the 59Fe labelling of this protein component were consistent with the changes observed in iron uptake by intact brush-border membrane vesicles. The 59Fe-labelling profiles of mucosal ferritin and transferrin from a test dose also were changed substantially in response to very-short-term alterations in dietary iron. Even though changes in dietary iron rapidly altered iron uptake by brush-border membrane vesicles and the incorporation of 59Fe from the test dose into mucosal transferrin, changes in the incorporation of 59Fe into mucosal ferritin best reflected the actual changes in the transfer of iron from dose to plasma.

SUBMITTER: Topham RW

PROVIDER: S-EPMC1132621 | biostudies-other | 1992 Jun

REPOSITORIES: biostudies-other

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Project description:There is increasing interest in utilizing short-term dietary interventions in the contexts of cancer, surgical stress and metabolic disease. These short-term diets may be more feasible than extended interventions and may be designed to complement existing therapies. In particular, the high-fat, low-carbohydrate ketogenic diet (KD), traditionally used to treat epilepsy, has gained popularity as a potential strategy for weight loss and improved metabolic health. In mice, long-term KD improves insulin sensitivity and may extend lifespan and healthspan. Dietary protein restriction (PR) causes increased energy expenditure, weight loss and improved glucose homeostasis. Since KD is inherently a low-protein diet (10% of calories from protein vs. >18% in control diet), here we evaluated the potential for mechanistic overlap between PR and KD via activation of a PR response. Mice were fed control, protein-free (PF), or one of four ketogenic diets with varying protein content for 8 days. PF and KD both decreased body weight, fat mass, and liver weights, and reduced fasting glucose and insulin levels, compared to mice fed the control diet. However, PF-fed animals had significantly improved insulin tolerance compared to KD. Furthermore, contrary to the PF-fed mice, mice fed ketogenic diets containing more than 5% of energy from protein did not increase hepatic Fgf21 or brown adipose Ucp1 expression. Interestingly, mice fed KD lacking protein demonstrated greater elevations in hepatic Fgf21 than mice fed a low-fat PF diet. To further elucidate potential mechanistic differences between PF and KD and the interplay between dietary protein and carbohydrate restriction, we conducted RNA-seq analysis on livers from mice fed each of the six diets and identified distinct gene sets which respond to dietary protein content, dietary fat content, and ketogenesis. We conclude that KD with 10% of energy from protein does not induce a protein restriction response, and that the overlapping metabolic benefits of KD and PF diets may occur via distinct underlying mechanisms.

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Alterations in the mucosal processing of iron in response to very-short-term dietary iron depletion and repletion.

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