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- Omar, Adila, 1985, et al.
(författare)
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Effects of High Intakes of Fructose and Galactose, with or without Added Fructooligosaccharides, on Metabolic Factors, Inflammation, and Gut Integrity in a Rat Model
- 2021
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Ingår i: Molecular Nutrition and Food Research. - : Wiley. - 1613-4125 .- 1613-4133. ; 65:6
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Tidskriftsartikel (refereegranskat)abstract
- Scope A high fructose and galactose intake show adverse metabolic effects in animal models and in humans, but it is yet unknown if addition of fermentable dietary fiber can mitigate such effects. This study investigate the effects of high intakes of fructose and galactose, with/without added fructooligosaccharides (FOS), on metabolic factors, inflammation, and gut integrity markers in rats. Methods and Results Rats (n = 6/group) receive different carbohydrates at isocaloric conditions for 12 weeks as follows: 1) starch (control), 2) fructose, 3) galactose, 4) starch + FOS (FOS control), 5) fructose + FOS, and 6) galactose + FOS, together with a high amount of n-6 polyunsaturated fatty acids (n-6 PUFA) in all diets except for in 7) starch + olive oil (negative control). The rats fed the galactose and galactose + FOS diets exhibit lower body weight than other groups. High-galactose diets has more pronounced effects on metabolic factors and gut permeability than high-fructose diets. High-fructose diets show less pronounced effect on these selected markers. No differences in inflammatory markers are detected for any of the diets. Conclusions The results suggest potential adverse effects of high galactose and fructose on metabolic factors and gut integrity markers, but not on inflammation. However, several mechanisms are at play, and general net effects are difficult to determine conclusively for the conditions tested.
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- Tata, Brooke, et al.
(författare)
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Elevated prenatal anti-Mullerian hormone reprograms the fetus and induces polycystic ovary syndrome in adulthood
- 2018
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Ingår i: Nature Medicine. - : Springer Science and Business Media LLC. - 1078-8956 .- 1546-170X. ; 24:6, s. 834-846
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Tidskriftsartikel (refereegranskat)abstract
- Polycystic ovary syndrome (PCOS) is the main cause of female infertility worldwide and corresponds with a high degree of comorbidities and economic burden. How PCOS is passed on from one generation to the next is not clear, but it may be a developmental condition. Most women with PCOS exhibit higher levels of circulating luteinizing hormone, suggestive of heightened gonadotropin-releasing hormone (GnRH) release, and anti-Mullerian hormone (AMH) as compared to healthy women. Excess AMH in utero may affect the development of the female fetus. However, as AMH levels drop during pregnancy in women with normal fertility, it was unclear whether their levels were also elevated in pregnant women with PCOS. Here we measured AMH in a cohort of pregnant women with PCOS and control pregnant women and found that AMH is significantly more elevated in the former group versus the latter. To determine whether the elevation of AMH during pregnancy in women with PCOS is a bystander effect or a driver of the condition in the offspring, we modeled our clinical findings by treating pregnant mice with AMH and followed the neuroendocrine phenotype of their female progeny postnatally. This treatment resulted in maternal neuroendocrine-driven testosterone excess and diminished placental metabolism of testosterone to estradiol, resulting in a masculinization of the exposed female fetus and a PCOS-like reproductive and neuroendocrine phenotype in adulthood. We found that the affected females had persistently hyperactivated GnRH neurons and that GnRH antagonist treatment in the adult female offspring restored their neuroendocrine phenotype to a normal state. These findings highlight a critical role for excess prenatal AMH exposure and subsequent aberrant GnRH receptor signaling in the neuroendocrine dysfunctions of PCOS, while offering a new potential therapeutic avenue to treat the condition during adulthood.
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