obsidian/🥙 Nutrition Vault/Fruit and liver fat.md
2024-09-14 08:39:18 -05:00

4.3 KiB
Executable file
Raw Permalink Blame History

Alami, Farkhondeh, et al. The Effect of a Fruit-Rich Diet on Liver Biomarkers, Insulin Resistance, and Lipid Profile in Patients with Non-Alcoholic Fatty Liver Disease: A Randomized Clinical TrialScandinavian Journal of Gastroenterology, June 2022, pp. 112. PubMed, https://doi.org/10.1080/00365521.2022.2071109.

Link: https://pubmed.ncbi.nlm.nih.gov/35710164/

Calorie Intake Differences: !

Notes:

Conclusions:

In conclusion, the present study found that 6 months of intervention with FRD exacerbated steatosis, dyslipidemia, and glycemic control of NAFLD patients. It is possible that excessive fruit consumption makes worse the condition of patients with fatty liver. According to the findings of the study, fruits intake increases the fat content of the hepatocyte probably through the lipogenic effect of fructose. To clarify the issue, more studies specifying a range for fruit intake (with minimum and maximum values) and considering obese patients and patients with different grades of fatty liver are warranted.

PDF: 📂 Media/PDFs/The effect of a fruit-rich diet on liver biomarkers, insulin resistance, and lipid profile in patients with non-alcoholic fatty liver disease- a randomized clinical trial.pdf

Supplements:

Endpoints Exposures Populations General People
#liver_enzymes #fruit #humans #nutrition
#insulin_sensitivity #clinical_trials
#blood_glucose #disease
#insulin #non_alcoholic_fatty_liver_disease
#clown_papers
#clownery

Johnston, Richard D., et al. No Difference Between High-Fructose and High-Glucose Diets on Liver Triacylglycerol or Biochemistry in Healthy Overweight MenGastroenterology, vol. 145, no. 5, Nov. 2013, pp. 1016-1025.e2. DOI.org (Crossref), https://doi.org/10.1053/j.gastro.2013.07.012.

Link: https://pubmed.ncbi.nlm.nih.gov/23872500/


Conclusions:

Features of NAFLD including steatosis, and elevated serum transaminases and triglycerides occurred during energy overfeeding. The present study reports no difference in these parameters between fructose and glucose. The greater uric acid concentration with fructose was evidence of a reduced pre pyruvate metabolic control, though it appears to have no hepatic impact in terms of hepatic volume, TAG storage, insulin resistance, glycogen synthesis, fasted ATP content, and biochemical assays of liver function. As such, any advice on low fructose diets in NAFLD remains unjustified. Further assessments are needed to assess if the energy overfeeding changes are monosaccharide specific, and to assess the outcomes of low monosaccharide intakes in NAFLD patients.

PDF: 📂 Media/PDFs/j.gastro.2013.07.012.pdf

Endpoints Exposures Populations General People
#non_alcoholic_fatty_liver_disease #glucose #humans #disease
#liver_enzymes #fructose #clinical_trials
#nutrition