Effects Of High Fructose Consumption Research Articles

Effect of high-fructose consumption in pregnancy on the bone growth of offspring rats.

Growing evidence suggests that bone health is programmed in early life. Maternal diet may influence the skeletal development of offspring. We aimed to determine the possible effects of high-fructose intake during pregnancy on different aspects of long bone morphology in the offspring of rats and to initially explore the possible mechanisms. Pregnant Sprague-Dawley rats were randomly divided into four groups and intragastrically administered the same dose of distilled water (CON, n = 12), 20 g/kg/day glucose (GLU, n = 12), 10 g/kg/day fructose (LFRU, n = 12), or 20 g/kg/day fructose (HFRU, n = 12) for 21 days during gestation. Computed tomography was used to analyze the cortical and cancellous bones of the distal femur of the offspring rats, and circulating bone metabolic biomarkers were measured using enzyme immunoassay. The results showed that high-fructose intake during pregnancy could decrease body weight, impair glucose metabolism, and increase serum leptin and uric acid in offspring. The offspring in the HFRU group had higher levels of the N-terminal propeptide of type I procollagen (PINP) and the C-telopeptide of type I collagen (CTX). The bone mean density (BMD), the total cross-sectional area inside the periosteal envelope (Tt.Ar), cortical bone area (Ct.Ar), medullary (or marrow) area (Ma.Ar), and trabecular mean density of the offspring in the HFRU group were lower than those in the CON group. Tartrate-resistant acid phosphatase (Trap) staining showed that high-fructose intake during pregnancy could increase the number of osteoclasts and increase the absorption area. Our results suggested that excessive fructose intake during pregnancy could inhibit skeletal development in offspring. Thus, attention to fructose intake during pregnancy is important for bone development in offspring.

Investigation of fructose consumption on hippocampal insulin and glucagon-like peptide-1 receptors, and metabolic effects in rats.

The detrimental effects of high fructose consumption on metabolic health have been extensively studied. However, limited research has focused on the impact of fructose intake on neuroprotective mechanisms, specifically the expression of insulin receptor (INSR) and glucagon-like peptide-1 receptor (GLP-1R) in the hippocampus. Understanding the effects of fructose on these neuroprotective molecules can provide valuable insights into the potential role of fructose in hippocampal dysfunction. The goal of this study is to aim at the basal plasma levels of lipid profile, insulin, GLP-1, and HOMA-IR, as well as the mRNA and protein expression of neuroprotective molecules such as INSR and GLP-1R in Wistar rats fed a high fructose diet. Rats were separated into control (C) and high fructose (HF) groups. The HF group was given 20% fructose water to drink for 16 weeks. Fructose ingestion significantly increased abdominal fat (C=1.24±0.08 g, HF=1.79±0.19 g, P<0.05) and plasma triglyceride levels (C=179.22±22.85 µg/ml, HF=242.45±14.45 µg/ml, P<0.05), but had no statistically significant effect on body weight and plasma HDL, LDL, total cholesterol, insulin, and GLP-1 levels (P>0.05). Although INSR mRNA expression in the hippocampus was significantly lower in the HF group compared to the control group (P<0.05), GLP-1R mRNA expression did not differ significantly across the groups (P>0.05). Furthermore, whereas INSR and GLP-1R protein levels in the experimental group were on a declining trend, this trend was not substantially different (P>0.05). These data suggest that fructose consumption may be harmful to the hippocampus by lowering the expression of INSR.

Maternal High-Fructose Intake Activates Myogenic Program in Fetal Brown Fat and Predisposes Offspring to Diet-Induced Metabolic Dysfunctions in Adulthood.

Excess dietary fructose intake is a major public health concern due to its deleterious effect to cause various metabolic and cardiovascular diseases. However, little is known about the effects of high-fructose consumption during pregnancy on offspring metabolic health in adulthood. Here, we show that maternal consumption of 20% (w/v) fructose water during pregnancy does not alter the metabolic balance of offspring with a chow diet, but predisposes them to obesity, fatty liver, and insulin resistance when challenged by a high-fat diet. Mechanistically, diet-induced brown fat reprogramming and global energy expenditure in offspring of fructose-fed dams are impaired. RNA-seq analysis of the fetal brown fat tissue reveals that the myogenic pathway is predominantly upregulated in the fructose-treated group. Meanwhile, circulating fructose level is found to be significantly elevated in both fructose-fed dams and their fetuses. Importantly fructose gavage also acutely activates the myogenic program in mice brown fat. Together, our data suggest that maternal high-fructose intake impairs fetal brown fat development, resultantly attenuates diet-induced thermogenesis and causes metabolic disorders in adult offspring probably through inducing myogenic signature in brown fat at the fetal stage.

Potential Therapeutic Activity of Mango (Mangifera indica L.) Leaves on Excess Consumption of Fructose in Rats

Background and Objective: High fructose consumption has increased worldwide. It causes various metabolic, genetic and histologic alterations. Alternative medicine, primarily herbal plants, has been proposed to alleviate the negative effects of high fructose consumption. The main objective of this study was to explore the efficacy of supplementation or treatment with mango leaves against high fructose induced alterations in male rats.&#x0D; Methodology: Mango leaves nutritional and active components were determined. A total of sixty male adult rats were used in this study. Fifteen rats were kept as healthy (negative control group; rats fed on balanced diet) while in others metabolic alterations were induced by consumption of high fructose diet ad libitum. Rats fed on high fructose diet were splited into 3 groups (15 rats in each), one group set as positive control group; rats fed on high fructose diet only and the other 2 groups; mango treated group; rats fed on high fructose diet until induction of hyperglycemia (one month and half) then fed on high fructose diet with replacement of fiber with 5% mango leaves and mango supplemented group; rats fed on high fructose diet with 5% mango leaves replacing fiber.&#x0D; Results: Mango leaves contain significant amounts of crude protein, crude fat, carbohydrates, crude fiber, ash, total flavonoids and polyphenols that controlled and corrected the following high fructose consumption results. Consumption of high fructose diet significantly (p≤0.05) increased final body weight (FBW), body weight gain (BWG), abdominal circumference (AC), Lee index and body mass index (BMI). High fructose also significantly (p≤0.05) increased levels of systolic blood pressure (SBP), serum triacylglycerol (TAG), total cholesterol (TC), fasting blood glucose, insulin, homeostasis model assessment-insulin resistance (HOMA-IR), serum tumor necrosis factor-α (TNF-α), leptin, malondialdehyde (MDA), advanced glycation end products (AGEs) and adipocyte size as well as blood histone deacetylase (HDAC) enzyme activity. High fructose consumption contrarily caused significant decrease (p≤0.05) in levels of quantitative insulin check index of insulin sensitivity (QUICKI), adiponectin, muscular insulin receptor substrate-1 (IRS-1) and glucose transporter-4 (GLUT-4) gene expression as well as blood reduced glutathione (GSH). Furthermore, microscopic examinations of the pancreatic and adipose tissues corroborated the biochemical findings.&#x0D; Conclusion: Mango leaves are a cheap source of macro and micronutrients as well as active constituents. By limiting metabolic and genetic abnormalities caused by high fructose consumption, either mango leaf supplementation or therapy improved and ameliorated all biochemical and microscopic data. The mango leaves supplemented group showed the most improvement.

High fructose-enriched diet synergistically exacerbates endocrine but not metabolic changes in letrozole-induced polycystic ovarian syndrome in Wistar rats

BackgroundPolycystic Ovarian Syndrome (PCOS) is a multifactorial endocrine-metabolic disorder that highly contributes to the prevalence of infertility globally. The increased consumption of refined carbohydrate, particularly fructose has been associated with pandemic metabolic disorders, including in women of reproductive age. However, the effects of high fructose consumption (FRD) on endocrine and metabolic disorders associated with PCOS are not clear. Therefore, this study investigated the effects of FRD on endocrine/metabolic changes in letrozole-induced PCOS in Wistar rats. Materials and methodsTwenty-eight adult female Wistar rats were randomly allotted into 4 groups and treated with vehicle, letrozole (LET; 0.5 mg/kg), FRD (D-fructose chow pellet mixture) and LET + FRD. The treatment lasted for 21days. ResultsData showed a significant increase in ovarian weight, liver weight, luteinising hormone (LH), testosterone and decrease in follicle stimulating hormone as well as moderate histopathological changes in the fallopian tube, uterus and liver of animals with PCOS. FRD-treated group showed a significant increase in ovarian weight and liver weight but no significant alteration in hormonal profile or histopathological changes in uterus and fallopian tube. However, FRD significantly altered hormonal profile with consequent histopathological changes in fallopian tube and uterus but FRD did not alter ovarian/liver weight or blood glucose in animals with PCOS when compared with animals without PCOS. ConclusionThe present results demonstrate that FRD synergistically aggravates endocrine but not metabolic changes in PCOS, suggesting that FRD might deteriorate endocrine-related phenotypes in PCOS.

Dietary (–)-epicatechin mitigates oxidative stress, NO metabolism alterations, and inflammation in renal cortex from fructose-fed rats

High fructose consumption has been associated to deleterious metabolic conditions. In the kidney, high fructose causes renal alterations that contribute to the development of chronic kidney disease. Evidence suggests that dietary flavonoids have the ability to prevent/attenuate risk factors of chronic diseases. This work investigated the capacity of (–)-epicatechin to prevent the renal damage induced by high fructose consumption in rats. Male Sprague Dawley rats received 10% (w/v) fructose in the drinking water for 8 weeks, with or without supplementation with (–)-epicatechin (20mg/kg body weight/d) in the rat chow diet. Results showed that, in the presence of mild proteinuria, the renal cortex from fructose-fed rats exhibited fibrosis and decreases in nephrin, synaptopodin, and WT1, all indicators of podocyte function in association with: (i) increased markers of oxidative stress; (ii) modifications in the determinants of NO bioavailability, i.e., NO synthase (NOS) activity and expression; and (iii) development of a pro-inflammatory condition, manifested as NF-κB activation, and associated with high expression of TNFα, iNOS, and IL-6. Dietary supplementation with (–)-epicatechin prevented or ameliorated the adverse effects of high fructose consumption. These results suggest that (–)-epicatechin ingestion would benefit when renal alterations occur associated with inflammation or metabolic diseases.

Glucocorticoid signaling in the liver and adipose tissue of male and female fructose-fed rats

Background The rise in consumption of refined sugars high in fructose appears to be an important factor contributing to epidemic of obesity and metabolic syndrome [1]. Fructose is involved in the genesis and progression of the syndrome through deregulation of metabolic pathways in the liver and adipose tissue, as sites of insulin-modulated metabolism [2]. Enhanced regeneration of glucocorticoids within the liver and adipose tissue, mediated by the enzyme 11beta-hydroxysteroid dehydrogenase type 1 (11bHSD1), may contribute to adiposity and metabolic disease [3]. 11bHSD1 reductase activity is crucially dependent on NADPH, a cofactor generated by the enzyme hexose-6phosphate dehydrogenase (H6PDH) [4]. We hypothesized that harmful effects of high fructose consumption are mediated by alterations in prereceptor metabolism of glucocorticoids and in the level of glucocorticoid receptor (GR) expression and compartmental redistribution in the liver and adipose tissue. We also assume that high fructose intake differently affects glucocorticoid signaling in the liver and adipose tissue of male and female rats.