Fructose, HFCS and Vitamin D - many studies
Both Fructose and HFCS (High Fructose Corn Syrup) reduce Vitamin D
both the tested and fully activated forms of Vitamin D
Vitamin D supplementation reduces problems resulting from Fructose or HFCS
15+ VitaminDWiki pages having FRUCTOSE OR HFCS in the title
This list is automatically updated
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Vitamin D supplement reduced some HFCS problems in rats - Feb 2024
Protective effect of vitamin D on learning and memory impairment in rats induced by high fructose corn syrup
Behavioural Brain Research Volume 459, 29 Feb 2024, 114763
https://doi.org/10.1016/j.bbr.2023.114763 PDF is behind a paywall
Cahide Aslan a 1, Rahime Aslankoc a, Ozlem Ozmen b, Buse Nur Sülük a, Oguzhan Kavrık a, Nurhan Gumral a
In our study, we aimed to investigate the negative effects of the prefrontal cortex (PFC)-associated impairment of cholinergic activity on memory and learning caused by high fructose corn syrup (HFCS) and the protective role of vitamin D in adolescent rats.
Twenty-four animals were divided into three groups as control, HFCS group (11 % HFCS-55 solution, ad libitum) and HFCS+ Vit D (42 μg/kg/day). Elevated Plus Maze (EPM), Forced Swim Test (FST), and Morris Water Maze (MWM, performed from day 23) tests were applied to all animals. Fluid intake consumption of the rats was measured daily, weight gain and blood glucose were measured weekly. After 31 days of treatment, the rats were sacrificed and PFC tissue was removed for biochemical, histopathological and immunohistochemical analyses.
In HFCS group, fluid consumption, blood glucose, malondialdehyde (MDA) levels, degenerative neuron count and choline acetyltransferase (ChAT) expression were significantly increased; superoxide dismutase (SOD), catalase (CAT) enzyme activity and brain-derived neurotrophic factor (BDNF) expression were significantly decreased. In addition, the time spent in the enclosed arm in EPM was increased, the immobility time in FST was, and the time spent in the target quadrant in MWM was significantly decreased. Vitamin D treatment reversed all these parameters. In conclusion, HFCS caused an increase in the number of degenerative neurons in the PFC, disrupted cholinergic activity and negatively affected learning-memory functions. Vitamin D, decreased the number of degenerative neurons, increased cholinergic activity and positively affected learning and memory performance.
Brief Synopsis
In this study, prefrontal cortex damage was investigated in adolescent rats fed high fructose corn syrup. The effect of vitamin D on prefrontal cortex damage was evaluated.
Vitamin D supplementation reduced problems of fructose-rich diets in mice - Sept 2019
The deficiency and the supplementation of vitamin D and liver: Lessons of chronic fructose-rich diet in mice
J of Steroid Biochemistry & Molecular Biology, Vol 192, Sep 2019, https://doi.org/10.1016/j.jsbmb.2019.105399
Thais C. Maia-Ceciliano, Rafaela R. Dutra, Marcia B. Aguila, Carlos A. Mandarim-De-Lacerda 1
Highlights
Vitamin D deficiency is growing at a global level and is linked to chronic diseases.
Fructose intake has a role in the epidemics of obesity and metabolic syndrome.
Fructose consumption plus vitamin D deficiency lead to steatosis and liver fibrosis.
Vitamin D supplementation lessen the adverse effects of the fructose intake.
The fructose added to soft drinks and processed food, as well as frequent detection of vitamin D deficiency in the body, are two insults increasingly considered to cause lesions in target organs. We studied the liver after a chronic high-fructose diet deficient and supplemented with vitamin D. Sixty C57BL/6 mature male mice were allocated into six groups (n = 10) for ten weeks: control (C), control deficient in vitamin D (CDD), control supplemented with vitamin D (CDS), fructose (F), fructose deficient in vitamin D (FDD), and fructose supplemented with vitamin D (FDS). The gene expressions of vitamin D receptor and CYP27B1 and 25 hydroxyvitamin D plasma level ensured that the diets caused vitamin D deficiency or supplementation. Body mass did not change, but blood pressure (BP) increased in CDD, F, and FDD, whereas BP was controlled in FDS. Insulinemia, insulin tolerance and resistance were seen in both vitamin D deficiency and fructose groups but improved with vitamin D supplementation. The steatosis and fibrosis were observed in the CDD, F and FDD groups. Also, F and FDD showed activation of stellate cells (HSC). Lipogenesis and inflammation gene expressions were enhanced in the CDD, F and FDD groups, but diminished with vitamin D supplementation. In conclusion, we demonstrated the adverse effects of vitamin D deficiency on metabolism, liver steatosis and, combined with fructose intake, liver interstitial fibrosis with hepatic stellate cell activation, and alteration of the lipogenesis, beta-oxidation, and liver inflammation. All these data improved when vitamin D was supplemented in the animals. 📄 Download the PDF from VitaminDWiki
Scientists claim to have found root cause of obesity for most people (HFCS) - Oct 2023
Daily Mail reporting on The fructose survival hypothesis as a mechanism for unifying the various obesity hypotheses
https://doi.org/10.1002/oby.23920 79 references online $12 to rent the PDF
The experts explained when people ingest fructose-heavy foods the amount of usable energy available to support the body’s cells plummets, leading to feelings of hunger.
Most carbs and fats people eat replace levels of ATP, a molecule that fuels cells so they can move, divide, and perform basic functions in the human body needed for survival.
This prompts the release of a hormone called leptin, which signals to the brain it’s time to stop eating.
But when fructose is metabolized in the liver, it uses ATP as an energy source. This causes fuel levels to plummet while at the same time interfering with the body’s ability to use stored fat as energy.
The reduction in ATP in cells is associated with hunger, thirst, increased food intake, reduced metabolism at rest, increased salt absorption, and more, all of which can lead to weight gain.
Fructose drives de novo lipogenesis affecting metabolic health - March 2023
in Journal of Endocrinology DOI: https://doi.org/10.1530/JOE-22-0270
Bettina Geidl-Flueck, Philipp A Gerber
Despite the existence of numerous studies supporting a pathological link between fructose consumption and the development of the metabolic syndrome and its sequelae, such as non-alcoholic fatty liver disease (NAFLD), this link remains a contentious issue. With this article, we shed a light on the impact of sugar/fructose intake on hepatic de novo lipogenesis (DNL), an outcome parameter known to be dysregulated in subjects with type 2 diabetes and/or NAFLD. In this review, we present findings from human intervention studies using physiological doses of sugar as well as mechanistic animal studies.
There is evidence from both human and animal studies that fructose is a more potent inducer of hepatic lipogenesis than glucose.
This is most likely due to the liver’s prominent physiological role in fructose metabolism, which may be disrupted under pathological conditions by increased hepatic expression of fructolytic and lipogenic enzymes.
Increased DNL may not only contribute to ectopic fat deposition (i.e. in the liver), but it may also impair several metabolic processes through DNL-related fatty acids (e.g. beta-cell function, insulin secretion, or insulin sensitivity).
📄 Download the PDF from VitaminDWiki
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VitaminDWiki – Obesity is associated with low Vitamin D (and treated by D as well) – Aug 2019 contains:
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