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You searched for subject:(alkaline diet). Showing records 1 – 2 of 2 total matches.

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Universiteit Utrecht

1. Brand, A.D. van den. On intestinal alkaline phosphatase and its role in high-fat diet-induced obesity.

Degree: 2014, Universiteit Utrecht

In this thesis, literature available on the adverse effects of a high fat diet on the integrity of the intestinal border is reviewed. In addition, the role of the enzyme alkaline phosphatase mediating in the process of fat absorption is evaluated. Dietary fat is absorbed via the enterocytes in the proximal part of the small intestine. This process of fat uptake is mediated by an enzyme intestinal alkaline phosphatase (IAP). Next to its regulatory role in fat absorption, IAP has immune-related properties. It is able to dephosphorylate bacterial lipopolysaccharide (LPS), thereby reducing its toxicity. However, after consuming a high fat diet (HFD), the composition of the gut microbiota is altered, favoring the presence of the LPS producing gram negative bacteria. Increased levels of LPS can cause a local inflammation, which can alter the epithelial lining of the gut wall by disturbing, for example, the tight junctions between the enterocytes. The HFD-induced rise in LPS levels, but also increased tension in the enterocytes due to the increased fat absorption can result in an increase in membrane permeability. Subsequently, LPS and pathogens can enter the blood, which may eventually result in endotoxemia. Thus, a HFD can cause a local as well as systemic inflammation, next to just an increased fat uptake. The increased level of fatty acids (FA) itself is also linked to a range of pathologies, as FA can interfere with the insulin signaling cascade. Defects in insulin action may result in insulin resistance, which has also been correlated with type 2 diabetes and liver cirrhosis. As IAP has a regulatory role in both fat uptake and LPS detoxification, it has an interesting therapeutic value. Therapeutic IAP may supplement the depletion of IAP due to an increase in fat absorption and LPS levels, induced by a HFD. This may restore the negative regulation IAP has on fat uptake, and may reduce the inflammatory responses initiated by LPS. Advisors/Committee Members: Kramer, Dr. Nynke I..

Subjects/Keywords: IAP; intestinal alkaline phosphatase; HFD; high fat diet; obesity; LPS; endotoxemia; insulin resistance

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Brand, A. D. v. d. (2014). On intestinal alkaline phosphatase and its role in high-fat diet-induced obesity. (Masters Thesis). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/297249

Chicago Manual of Style (16th Edition):

Brand, A D van den. “On intestinal alkaline phosphatase and its role in high-fat diet-induced obesity.” 2014. Masters Thesis, Universiteit Utrecht. Accessed January 16, 2021. http://dspace.library.uu.nl:8080/handle/1874/297249.

MLA Handbook (7th Edition):

Brand, A D van den. “On intestinal alkaline phosphatase and its role in high-fat diet-induced obesity.” 2014. Web. 16 Jan 2021.

Vancouver:

Brand ADvd. On intestinal alkaline phosphatase and its role in high-fat diet-induced obesity. [Internet] [Masters thesis]. Universiteit Utrecht; 2014. [cited 2021 Jan 16]. Available from: http://dspace.library.uu.nl:8080/handle/1874/297249.

Council of Science Editors:

Brand ADvd. On intestinal alkaline phosphatase and its role in high-fat diet-induced obesity. [Masters Thesis]. Universiteit Utrecht; 2014. Available from: http://dspace.library.uu.nl:8080/handle/1874/297249


University of New South Wales

2. Kozan, Pinar. The effect of buffering a high acid load meal with sodium bicarbonate on postprandial glucose metabolism in humans.

Degree: St Vincent's Clinical School, 2018, University of New South Wales

Background: High dietary acid load relates to increased risk of type 2 diabetes in epidemiological studies. We aimed to investigate whether buffering a high acid load meal with an alkalising treatment changes post meal glucose metabolism. Methods: Non-diabetic participants (n=32) were randomized to receive either NaHCO3 1680mg or placebo, followed by a high acid load meal in a double-blind placebo-controlled crossover (1-4 weeks apart) study. Thirty (20 males) participants completed the study. Venous blood pH, serum bicarbonate, blood glucose, serum insulin, C-peptide, non-esterified fatty acid (NEFA), and plasma glucagon-like peptide-1 (GLP-1) concentrations were measured at baseline (fasting) and at 15-30min intervals for 3h post meal. Results: The treatment was well tolerated. Venous blood pH declined in the first 15min post meal with the placebo (p=0.001), but not with NaHCO3 (p=0.86) and remained lower with the placebo for 3h (pinteraction=0.04). The iAUC of pH was significantly higher following the NaHCO3 treatment versus the placebo (p=0.02). However, postprandial glucose, insulin, C-peptide, NEFA and GLP-1 were not different between treatments (pinteraction‚Č•0.07). Conclusions: An alkalising medication administered pre-meal has no acute effect on glycaemia and insulin response in healthy individuals. Long-term interventions in at-risk populations are necessary to investigate the effect of sustained alkalisation on glucose metabolism. Advisors/Committee Members: Greenfield , Jerry, Garvan Institute of Medical Research, Faculty of Medicine, UNSW, Samocha-Bonet, Dorit, Garvan Institute of Medical Research, Faculty of Medicine, UNSW.

Subjects/Keywords: acid-base homeostasis; alkaline diet; dietary acid load; type 2 diabetes; sodium bicarbonate; postprandial glycaemia

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Kozan, P. (2018). The effect of buffering a high acid load meal with sodium bicarbonate on postprandial glucose metabolism in humans. (Masters Thesis). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/59592 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:49042/SOURCE02?view=true

Chicago Manual of Style (16th Edition):

Kozan, Pinar. “The effect of buffering a high acid load meal with sodium bicarbonate on postprandial glucose metabolism in humans.” 2018. Masters Thesis, University of New South Wales. Accessed January 16, 2021. http://handle.unsw.edu.au/1959.4/59592 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:49042/SOURCE02?view=true.

MLA Handbook (7th Edition):

Kozan, Pinar. “The effect of buffering a high acid load meal with sodium bicarbonate on postprandial glucose metabolism in humans.” 2018. Web. 16 Jan 2021.

Vancouver:

Kozan P. The effect of buffering a high acid load meal with sodium bicarbonate on postprandial glucose metabolism in humans. [Internet] [Masters thesis]. University of New South Wales; 2018. [cited 2021 Jan 16]. Available from: http://handle.unsw.edu.au/1959.4/59592 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:49042/SOURCE02?view=true.

Council of Science Editors:

Kozan P. The effect of buffering a high acid load meal with sodium bicarbonate on postprandial glucose metabolism in humans. [Masters Thesis]. University of New South Wales; 2018. Available from: http://handle.unsw.edu.au/1959.4/59592 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:49042/SOURCE02?view=true

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