Consumption Of High Sugar Diet Research Articles

Early-Life Sugar Consumption Affects the Microbiome in Juvenile Mice.

The composition of the gut microbiota is influenced by the dietary nutrient. Sugar has been linked with many metabolic health disorders such as heart disease, metabolic syndrome, and immune disorders. Long-term consumption of sugar influences the landscape of gut microbiota by altering the gut microbial population called dysbiosis. This study aims to evaluate the impact of long-term consumption of high sugar diet (HSD) on the diversity of gut microbiota. CD1 mice are given high concentration of sugar for 15weeks followed by a recovery period of 10weeks. Real-time polymerase chain reaction and 16S rRNA next-generation sequencing methods employ to identify microbiome diversity. The results show that Firmicutes and Bacteroidetes are the predominant phyla in control, cecum, and fecal samples. Firmicutes population are gradually increased in treated samples even after the recovery period, whereas Bacteroidetes abundance slightly reduces throughout the study. The present study shows that the impact of long period of high sugar diet consumption alters the diversity of normal gut flora which can be restored after 10weeks of sugar withdrawal. This indicates that the intervention of healthy and nutritious diet influences gut microbes and this can be beneficial in reducing the implication of early life metabolic disorders such as obesity.

Autophagy and Glycative Stress: A Bittersweet Relationship in Neurodegeneration.

Autophagy is a fine-tuned proteolytic pathway that moves dysfunctional/aged cellular components into the lysosomal compartment for degradation. Over the last 3 decades, global research has provided evidence for the protective role of autophagy in different brain cell components. Autophagic capacities decline with age, which contributes to the accumulation of obsolete/damaged organelles and proteins and, ultimately, leads to cellular aging in brain tissues. It is thus well-accepted that autophagy plays an essential role in brain homeostasis, and malfunction of this catabolic system is associated with major neurodegenerative disorders. Autophagy function can be modulated by different types of stress, including glycative stress. Glycative stress is defined as a cellular status with abnormal and accelerated accumulation of advanced glycation end products (AGEs). It occurs in hyperglycemic states, both through the consumption of high-sugar diets or under metabolic conditions such as diabetes. In recent years, glycative stress has gained attention for its adverse impact on brain pathology. This is because glycative stress stimulates insoluble, proteinaceous aggregation that is linked to the malfunction of different neuropathological proteins. Despite the emergence of new literature suggesting that autophagy plays a major role in fighting glycation-derived damage by removing cytosolic AGEs, excessive glycative stress might also negatively impact autophagic function. In this mini-review, we provide insight on the status of present knowledge regarding the role of autophagy in brain physiology and pathophysiology, with an emphasis on the cytoprotective role of autophagic function to ameliorate the adverse effects of glycation-derived damage in neurons, glia, and neuron-glia interactions.

High-sugar diet leads to obesity and metabolic diseases in ad libitum -fed rats irrespective of caloric intake.

Objective Provide a comprehensive view of the events surrounding the sugar consumption, under conditions of energy equivalence; through the analysis of behavioral aspects of intake, and of biochemical, metabolic and physiological parameters, as well as the effect of this nutrient on the plasticity of adipose tissue. Materials and methods Newly weaned male Wistar rats were classified in two groups and subjected to the following normocaloric diets: standard chow diet or to high-sugar diet (HSD) ad libitum for 18 weeks. Results The animals submitted to the HSD were associated with a lower caloric intake during the 18 weeks of experimentation. However, the HSD induced a significant increase in body weight, white adipose tissue weight, adiposity index, Lee index, and the levels of triglycerides and very low-density lipoprotein in the serum. In addition, it induced glucose intolerance, insulin resistance and compensatory increase of insulin secretion by pancreatic β-cells. Also increased heart rate and induced hyperplasia, and hypertrophy of retroperitoneal visceral adipose tissue. In the liver, the HSD was associated with increased hepatic lipid content (i.e., triglycerides and cholesterol) and hepatomegaly. Conclusion The post-weaning consumption of HSD induces an adaptive response in metabolism; however, such an event is not enough to reverse the homeostatic imbalance triggered by the chronic consumption of this macronutrient, leading to the development of metabolic syndrome, irrespective of caloric intake. These findings corroborate recent evidence indicating that sugar is a direct contributor to metabolic diseases independent of a positive energy balance. Arch Endocrinol Metab. 2020;64(1):71-81.

Cardioprotective effect of Phyllanthus amarus against high fructose diet induced myocardial and aortic stress in rat model

Increased number of population with heart stroke/attack is attributed to sedentary lifestyle and consumption of high-sugar diets, especially fructose. The objective of this study is to investigate the cardio-protective activity of aqueous extract of Phyllanthus amarus (PAAE) against high-fructose (HF) diet induced cardiac damage in Wistar rats. Male Wistar rats were randomly assigned into five groups of six animals each: Control (C), Control treated with PAAE (C+PAAE), High fructose diet fed (F), High fructose diet fed treated with PAAE (F+PAAE) and High fructose diet fed treated with Pioglitazone (F+Pio). PAAE was orally administered at a dosage of 200mg/kg body weight/day to C+PAAE and F+PAAE group rats for 60days. Pioglitazone (10mg/kg body weight/day) was used to compare the efficacy of PAAE. After 60days, heart and aorta samples were collected for biochemical and histological analysis. Co-administration of PAAE along with HF-diet for 60days prevented the increase in levels of cardiac and aortic lipids i.e., total lipids, triglycerides, total cholesterol and free fatty acids and decreased phospholipids. Further, enhanced activities of cardiac aldose reductase (15.3%) and sorbital dehydrogenase (6.9%) and decreased activity of creatine kinase (35.6%) in group-F were also prevented by PAAE treatment with the recovery of 126% for AR, 122% for SDH and 118% for CK. PAAE treatment showed protection from HF-diet induced increase in stress markers (LPO and PO), decreased non-enzymatic (GSH and Vit-C) and enzymatic (GR, GPx, GST, SOD, and CAT) antioxidants in the heart and aorta. Histopathological examination of the heart and aorta indicated that PAAE/Pio treatment reduced fat deposition and necrosis. The present study clearly indicates the cardio protection efficacy of PAAE against HF-diet induced oxidative stress in rats.