Fructose-induced inflammation and increased cortisol: A new mechanism for how sugar induces visceral adiposity
- PMID: 29225114
- DOI: 10.1016/j.pcad.2017.12.001
Fructose-induced inflammation and increased cortisol: A new mechanism for how sugar induces visceral adiposity
Abstract
Traditionally, the leading hypothesis regarding the development of obesity involves caloric imbalance, whereby the amount of calories consumed exceeds the amount of calories burned which causes obesity. Another hypothesis for why we get fat has surfaced in the last decade which is the idea that the overconsumption of added sugars and refined carbohydrates induce insulin resistance and high insulin levels causing obesity. While insulin is a fat-storing hormone, this hypothesis does not explain visceral adiposity, or why certain people are found to have fat stored in and around their organs. We propose a new mechanism for body fattening, particular visceral adiposity. This hypothesis involves the overconsumption of fructose, which leads to inflammation in all cells that metabolize it rapidly. When fructose is metabolized in subcutaneous adipocytes, the subsequent inflammation leads to an increase in intracellular cortisol in order to help squelch the inflammation. Unfortunately, the increase in intracellular cortisol leads to an increased flux of fatty acids out of the subcutaneous adipocytes allowing more substrate for fat storage into visceral fat tissue. Moreover fructose-induced inflammation in the liver also leads to increased intracellular cortisol via an upregulation of 11-B hydroxysteroid dehydrogenase type 1 causing increased fat storage in the liver (i.e., fatty liver). In essence, the fructose-induced inflammatory cortisol response causes "thin on the outside, fat on the inside" (TOFI). Furthermore, fructose in the brain, either from fructose uptake via the blood brain barrier or endogenous formation from glucose via the polyol pathway stimulates an increased release of cortisol causing hepatic gluconeogenesis leading to overall insulin resistance and further body fattening. This review paper will discuss in detail the hypothesis that fructose-induced inflammation and cortisol activation causes visceral adiposity.
Keywords: Cortisol; Fat; Fructose; Inflammation; Obesity; Sugar; Visceral adiposity.
Copyright © 2017 Anesthesia History Association. Published by Elsevier Inc. All rights reserved.
Similar articles
-
Chronic fructose intake accelerates non-alcoholic fatty liver disease in the presence of essential hypertension.J Diabetes Complications. 2016 Jan-Feb;30(1):85-92. doi: 10.1016/j.jdiacomp.2015.10.008. Epub 2015 Oct 19. J Diabetes Complications. 2016. PMID: 26597602
-
Effect of trans-fat, fructose and monosodium glutamate feeding on feline weight gain, adiposity, insulin sensitivity, adipokine and lipid profile.Br J Nutr. 2011 Jul;106(2):218-26. doi: 10.1017/S000711451000588X. Br J Nutr. 2011. PMID: 21429276
-
Fructose-enriched diet induces inflammation and reduces antioxidative defense in visceral adipose tissue of young female rats.Eur J Nutr. 2017 Feb;56(1):151-160. doi: 10.1007/s00394-015-1065-0. Epub 2015 Oct 3. Eur J Nutr. 2017. PMID: 26433940
-
Fructose and hepatic insulin resistance.Crit Rev Clin Lab Sci. 2020 Aug;57(5):308-322. doi: 10.1080/10408363.2019.1711360. Epub 2020 Jan 14. Crit Rev Clin Lab Sci. 2020. PMID: 31935149 Free PMC article. Review.
-
The role of dietary sugars and de novo lipogenesis in non-alcoholic fatty liver disease.Nutrients. 2014 Dec 10;6(12):5679-703. doi: 10.3390/nu6125679. Nutrients. 2014. PMID: 25514388 Free PMC article. Review.
Cited by
-
Visceral Adipose Tissue: The Hidden Culprit for Type 2 Diabetes.Nutrients. 2024 Mar 30;16(7):1015. doi: 10.3390/nu16071015. Nutrients. 2024. PMID: 38613048 Free PMC article. Review.
-
Effect of Exercise Conditioning on Countering the Effects of Obesity and Insulin Resistance in Horses-A Review.Animals (Basel). 2024 Feb 26;14(5):727. doi: 10.3390/ani14050727. Animals (Basel). 2024. PMID: 38473112 Free PMC article. Review.
-
Effects of Halloysite Nanotubes and Multi-walled Carbon Nanotubes on Kruppel-like Factor 15-Mediated Downstream Events in Mouse Hearts After Intravenous Injection.Cardiovasc Toxicol. 2024 Apr;24(4):408-421. doi: 10.1007/s12012-024-09844-7. Epub 2024 Feb 27. Cardiovasc Toxicol. 2024. PMID: 38411850
-
Assessing Metabolic Differences Associated with Exposure to Polybrominated Biphenyl and Polychlorinated Biphenyls in the Michigan PBB Registry.Environ Health Perspect. 2023 Oct;131(10):107005. doi: 10.1289/EHP12657. Epub 2023 Oct 10. Environ Health Perspect. 2023. PMID: 37815925 Free PMC article.
-
The impact of dietary fructose on gut permeability, microbiota, abdominal adiposity, insulin signaling and reproductive function.Heliyon. 2023 Aug 9;9(8):e18896. doi: 10.1016/j.heliyon.2023.e18896. eCollection 2023 Aug. Heliyon. 2023. PMID: 37636431 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical