Hormonal
High glycemic index (GI) carbohydrates induce metabolic damage primarily through rapid glucose absorption in the proximal small intestine, which stimulates GIP release from K cells, leading to lipogenesis, fatty liver, insulin resistance, and inflammation, whereas low GI carbohydrates bypass this mechanism.
To minimize metabolic damage from carbohydrates, prioritize foods with a low glycemic index (like isomaltulose, legumes, or whole grains) over high GI foods (like sucrose or white bread). This is because high GI foods are rapidly absorbed in the upper intestine, triggering GIP release which promotes fat storage, liver fat, and inflammation. Low GI foods are absorbed more slowly, bypassing the GIP-triggering K cells and instead stimulating beneficial GLP-1 release.
When glucose–fructose dimers are supplied as the slowly digestible, completely absorbable, low glycemic index (GI) sugar isomaltulose, the detrimental effects of high GI sucrose are avoided. This difference requires the presence of intact glucose-induced insulinotropic peptide receptor (GIPR) and is mediated by the rapid uptake of glucose and the stimulation of GIP release from K cells in the upper small intestine. GIP promotes lipogenesis, fatty liver, insulin resistance, and postprandial inflammation, and reduces fat oxidation in skeletal muscle...
Why this rating
Supported by multiple human intervention studies comparing sucrose vs. isomaltulose and genetic mouse models (GIPR-/-), though it is an opinion/review paper synthesizing these findings.
Source
High Glycemic Index Metabolic Damage – a Pivotal Role of GIP and GLP-1
Andreas Pfeiffer et al. · Trends in Endocrinology and Metabolism · 2018
DOI 10.1016/j.tem.2018.03.003
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