Oxidative and endoplasmic reticulum stress develop adverse metabolic effects due to the high-fat high-fructose diet consumption from birth to young adulthood

High‐fat, high‐sucrose, and combined high‐fat/high‐sucrose diets effects in oxidative stress and inflammation in male rats under presence or absence of obesity

“…The condition of insulin resistance, hyperglycemia, and the consequent overload of intracellular glucose increase via glycolysis, as well as the proton gradient across the inner mitochondrial membrane, leading to an escape of electrons with superoxide anion formation (Choi et al, 2008 ). Hyperleptinemia, in turn, is responsible for the activation of macrophages, production of TNF‐α and NO synthase, in addition to the proliferation and migration of endothelial cells, resulting in increased superoxide generation (Izadi et al, 2022 ; Mangge et al, 2017 ). Izadi et al ( 2022 ) have shown that high‐fat high‐fructose diet promotes elevation of plasma leptin level and the hypothalamic leptin content, oxidative stress marker (through the MDA level increment), indicating that the rise of pro‐inflammatory metabolites is induced through the high‐fat high‐fructose consumption and stimulates leptin secretion.…”

“…Hyperleptinemia, in turn, is responsible for the activation of macrophages, production of TNF‐α and NO synthase, in addition to the proliferation and migration of endothelial cells, resulting in increased superoxide generation (Izadi et al, 2022 ; Mangge et al, 2017 ). Izadi et al ( 2022 ) have shown that high‐fat high‐fructose diet promotes elevation of plasma leptin level and the hypothalamic leptin content, oxidative stress marker (through the MDA level increment), indicating that the rise of pro‐inflammatory metabolites is induced through the high‐fat high‐fructose consumption and stimulates leptin secretion. The increased leptin level stimulates ROS production and induces oxidative stress (Berger & Polotsky, 2018 ).…”

The possible mechanisms of high-fructose diet-induced pancreatic disturbances

“…Similarly, the expression of ER stress-related proteins, including IRE1, PERK, and activating transcription factor 6 (ATF6) were increased in the pancreatic tissue of high-fat/high-fructose-fed rats [52]. Also, it was determined an increase in oxidative parameters, including CAT, glutathione (GSH), and MDA as well as ER stress-related proteins such as binding immunoglobulin protein (BIP) and CHOP in the pancreas of rats fed with a high-fat/high-fructose diet from birth to young adulthood [18]. In conclusion, cellular stress factors may play an important role in pancreatic dysfunction of T2D and high-fructose-induced metabolic disorder.…”

“…In the pancreatic tissue, high-fructose-induced hyperglycemia may lead to the activation of cellular stress and mitogenic pathways thereby leading to a high secretion capacity of β-cells. Dietary fructose may also trigger pancreatic inflammation and β-cell death during the disease progression [17,18]. Thus, dietary fructose may cause structural and functional disturbances in β-cells.…”