Central and Metabolic Effects of High Fructose Consumption: Evidence from Animal and Human Studies
Fructose consumption has increased dramatically in the last 40 years, and its role in the pathogenesis of the metabolic syndrome has been implicated by many studies. It is most often encountered in the diet as sucrose (glucose and fructose) or high-fructose corn syrup (55% fructose). At high levels,...
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Shahid Beheshti University of Medical Sciences
2014-12-01
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doaj-04de61ddae434cd2b35f3f06592f1f4f2020-11-24T22:10:07ZengShahid Beheshti University of Medical SciencesNutrition and Food Sciences Research2283-04412383-30092014-12-011239Central and Metabolic Effects of High Fructose Consumption: Evidence from Animal and Human StudiesAlexandra Stoianov0Khosrow Adeli1 Fructose consumption has increased dramatically in the last 40 years, and its role in the pathogenesis of the metabolic syndrome has been implicated by many studies. It is most often encountered in the diet as sucrose (glucose and fructose) or high-fructose corn syrup (55% fructose). At high levels, dietary exposure to fructose triggers a series of metabolic changes originating in the liver, leading to hepatic steatosis, hypertriglyceridemia, insulin resistance, and decreased leptin sensitivity. Fructose has been identified to alter biological pathways in other tissues including the central nervous system (CNS), adipose tissue, and the gastrointestinal system. Unlike glucose, consumption of fructose produces smaller increases in the circulating satiety hormone glucagon-like peptide 1 (GLP-1), and does not attenuate levels of the appetite suppressing hormone ghrelin. In the brain, fructose contributes to increased food consumption by activating appetite and reward pathways, and stimulating hypothalamic AMPK activity, a nutrient-sensitive regulator of food intake. Recent studies investigating the neurophysiological factors linking fructose consumption and weight gain in humans have demonstrated differential activation of brain regions that govern appetite, motivation and reward processing. Compared to fructose, glucose ingestion produces a greater reduction of hypothalamic neuronal activity, and increases functional connectivity between the hypothalamus and other reward regions of the brain, indicating that these two sugars regulate feeding behavior through distinct neural circuits. This review article outlines the current findings in fructose-feeding studies in both human and animal models, and discusses the central effects on the CNS that may lead to increased appetite and food intake. Keywords: Fructose, Metabolic syndrome, Appetite, Central nervous systemhttp://nfsr.sbmu.ac.ir/browse.php?a_code=A-10-1-4&slc_lang=en&sid=1Fructose Metabolic syndrome Appetite Central nervous system |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Alexandra Stoianov Khosrow Adeli |
spellingShingle |
Alexandra Stoianov Khosrow Adeli Central and Metabolic Effects of High Fructose Consumption: Evidence from Animal and Human Studies Nutrition and Food Sciences Research Fructose Metabolic syndrome Appetite Central nervous system |
author_facet |
Alexandra Stoianov Khosrow Adeli |
author_sort |
Alexandra Stoianov |
title |
Central and Metabolic Effects of High Fructose Consumption: Evidence from Animal and Human Studies |
title_short |
Central and Metabolic Effects of High Fructose Consumption: Evidence from Animal and Human Studies |
title_full |
Central and Metabolic Effects of High Fructose Consumption: Evidence from Animal and Human Studies |
title_fullStr |
Central and Metabolic Effects of High Fructose Consumption: Evidence from Animal and Human Studies |
title_full_unstemmed |
Central and Metabolic Effects of High Fructose Consumption: Evidence from Animal and Human Studies |
title_sort |
central and metabolic effects of high fructose consumption: evidence from animal and human studies |
publisher |
Shahid Beheshti University of Medical Sciences |
series |
Nutrition and Food Sciences Research |
issn |
2283-0441 2383-3009 |
publishDate |
2014-12-01 |
description |
Fructose consumption has increased dramatically in the last 40 years, and its role in the pathogenesis of the metabolic syndrome has been implicated by many studies. It is most often encountered in the diet as sucrose (glucose and fructose) or high-fructose corn syrup (55% fructose). At high levels, dietary exposure to fructose triggers a series of metabolic changes originating in the liver, leading to hepatic steatosis, hypertriglyceridemia, insulin resistance, and decreased leptin sensitivity. Fructose has been identified to alter biological pathways in other tissues including the central nervous system (CNS), adipose tissue, and the gastrointestinal system. Unlike glucose, consumption of fructose produces smaller increases in the circulating satiety hormone glucagon-like peptide 1 (GLP-1), and does not attenuate levels of the appetite suppressing hormone ghrelin. In the brain, fructose contributes to increased food consumption by activating appetite and reward pathways, and stimulating hypothalamic AMPK activity, a nutrient-sensitive regulator of food intake. Recent studies investigating the neurophysiological factors linking fructose consumption and weight gain in humans have demonstrated differential activation of brain regions that govern appetite, motivation and reward processing. Compared to fructose, glucose ingestion produces a greater reduction of hypothalamic neuronal activity, and increases functional connectivity between the hypothalamus and other reward regions of the brain, indicating that these two sugars regulate feeding behavior through distinct neural circuits. This review article outlines the current findings in fructose-feeding studies in both human and animal models, and discusses the central effects on the CNS that may lead to increased appetite and food intake.
Keywords: Fructose, Metabolic syndrome, Appetite, Central nervous system |
topic |
Fructose Metabolic syndrome Appetite Central nervous system |
url |
http://nfsr.sbmu.ac.ir/browse.php?a_code=A-10-1-4&slc_lang=en&sid=1 |
work_keys_str_mv |
AT alexandrastoianov centralandmetaboliceffectsofhighfructoseconsumptionevidencefromanimalandhumanstudies AT khosrowadeli centralandmetaboliceffectsofhighfructoseconsumptionevidencefromanimalandhumanstudies |
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