High-fat And High-sugar Research Articles

Association between Take-Out Food Consumption and Obesity among Chinese University Students: A Cross-Sectional Study.

Background: The frequency of take-out food consumption has increased rapidly among Chinese college students, which has contributed to high obesity prevalence. However, the relationships between take-out food consumption, body mass index (BMI), and other individual factors influencing eating behavior among college students are still unclear. This study explored the association of take-out food consumption with gender, BMI, physical activity, preference for high-fat and high-sugar (HFHS) food, major category, and degree level among Chinese college students. Methods: Cross-sectional data were collected from 1220 college students in Beijing, China, regarding information about take-out food consumption, physical activity, and preference for HFHS food using a self-reported questionnaire. The logistic linear regression model was used to analyze the association between take-out food consumption and personal and lifestyle characteristics. Results: Out of 1220 college students, 11.6% of college students were overweight or obese. Among the personal and lifestyle characteristics, high frequency of take-out food consumption was significantly associated with a non-medical major, high preference for HFHS food, degree level, and higher BMI, but not physical activity. Conclusion: Among Chinese college students, consumption of take-out food may be affected by major category, preference for HFHS food, degree level, and BMI. This could provide guidance on restrictions of high take-out food consumption, which contributes to high obesity prevalence and high risk for metabolic diseases.

An intermittent hypercaloric diet alters gut microbiota, prefrontal cortical gene expression and social behaviours in rats

Objectives: Excessive consumption of high fat and high sugar (HFHS) diets alters reward processing, behaviour, and changes gut microbiota profiles. Previous studies in gnotobiotic mice also provide evidence that these gut microorganisms may influence social behaviour. To further investigate these interactions, we examined the impact of the intermittent access to a HFHS diet on social behaviour, gene expression and microbiota composition in adolescent rats. Methods: Male rats were permitted intermittent daily access (2 h / day) to a palatable HFHS chow diet for 28 days across adolescence. Social interaction, social memory and novel object recognition were assessed during this period. Following testing, RT-PCR was conducted on hippocampal and prefrontal cortex (PFC) samples. 16S ribosomal RNA amplicon sequencing was used for identification and relative quantification of bacterial taxa in faecal samples. Results: We observed reduced social interaction behaviours, impaired social memory and novel object recognition in HFHS diet rats compared to chow controls. RT-PCR revealed reduced levels of monoamine oxidase A (Maoa), catechol-O-methyltransferase (Comt) and brain derived neurotrophic factor (Bdnf) mRNA in the PFC of HFHS diet rats. Faecal microbiota analysis demonstrated that the relative abundance of a number of specific bacterial taxa differed significantly between the two diet groups, in particular, Lachnospiraceae and Ruminoccoceae bacteria. Discussion: Intermittent HFHS diet consumption evoked physiological changes to the brain, particularly expression of mRNA associated with reward and neuroplasticity, and gut microbiome. These changes may underpin the observed alterations to social behaviours.

Comparative analysis of fecal phenolic content between normal and obese rats after oral administration of tea polyphenols.

Tea polyphenols (TP) have many health benefits, but most are metabolized into low molecular-weight phenolic acids after oral administration. In the present study, the absorption, metabolism, and excretion of catechins in rats fed a normal chow diet and in obese rats fed a high-fat and high-sugar (HFHS) diet were compared. After a ten-day oral administration of TP (500 mg per kg bw), the plasma levels of (-)-epigallocatechin gallate (EGCG) and (-)-gallocatechin gallate (GCG) in obese rats were significantly lower than those in the normal group. In obese rats, the fecal levels of EGCG, (-)-epicatechin gallate (ECG) and GCG were significantly enhanced. Ten phenolic metabolites of TP were quantitatively analyzed, and the results showed that 4-hydroxyphenylacetic acid was the primary metabolite in feces and plasma. The plasma and fecal concentrations of 4-hydroxyphenylacetic acid in the obese group were significantly lower than those in normal rats, but the levels of 4-hydroxyphenylpropionic acid in plasma and feces were increased. The content of other phenolic acids was also dramatically changed. These results suggested that a HFHS diet might influence the excretion of tea catechins, leading to insufficient metabolism of catechins by the gut microflora.

A Western-style obesogenic diet alters maternal metabolic physiology with consequences for fetal nutrient acquisition in mice.

Key points In the Western world, obesogenic diets containing high fat and high sugar (HFHS) are commonly consumed during pregnancy, although their effects on the metabolism of the mother, in relation to feto‐placental glucose utilization and growth, are unknown.In the present study, the consumption of an obesogenic HFHS diet compromised maternal glucose tolerance and insulin sensitivity in late pregnancy in association with dysregulated lipid and glucose handling by the dam.These maternal metabolic changes induced by HFHS feeding were related to altered feto‐placental glucose metabolism and growth.A HFHS diet during pregnancy therefore causes maternal metabolic dysfunction with consequences for maternal nutrient allocation for fetal growth.These findings have implications for the health of women and their infants, who consume obesogenic diets during pregnancy. In the Western world, obesogenic diets containing high fat and high sugar (HFHS) are commonly consumed during pregnancy. However, the impacts of a HFHS diet during pregnancy on maternal insulin sensitivity and signalling in relation to feto‐placental growth and glucose utilization are unknown. The present study examined the effects of a HFHS diet during mouse pregnancy on maternal glucose tolerance and insulin resistance, as well as, on feto‐placental glucose metabolism. Female mice were fed a control or HFHS diet from day (D) 1 of pregnancy (term = D20.5). At D16 or D19, dams were assessed for body composition, metabolite and hormone concentrations, tissue abundance of growth and metabolic signalling pathways, glucose tolerance and utilization and insulin sensitivity. HFHS feeding perturbed maternal insulin sensitivity in late pregnancy; hepatic insulin sensitivity was higher, whereas sensitivity of the skeletal muscle and white adipose tissue was lower in HFHS than control dams. These changes were accompanied by increased adiposity and reduced glucose production and glucose tolerance of HFHS dams. The HFHS diet also disturbed the hormone and metabolite milieu and altered expression of growth and metabolic signalling pathways in maternal tissues. Furthermore, HFHS feeding was associated with impaired feto‐placental glucose metabolism and growth. A HFHS diet during pregnancy therefore causes maternal metabolic dysfunction with consequences for maternal nutrient allocation for fetal growth. These findings have implications for the health of women and their infants, who consume HFHS diets during pregnancy.

Fat-1 mice prevent high-fat plus high-sugar diet-induced non-alcoholic fatty liver disease.

High-fat and high-sugar (HFS) diets have been suggested to play a causal role in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). This study aimed to investigate whether fat-1 transgenic mice with a higher tissue content of n-3 polyunsaturated fatty acids (PUFAs) could prevent HFS diet-induced NAFLD, compared with wild-type mice. The fat-1 and wild-type littermates had free access to a 15% fructose solution plus high-fat diet, a 15% glucose solution plus high-fat diet, or a 15% sucrose solution plus high-fat diet, respectively. Caloric intake, weight gain, biochemical parameters, histology, and gene and protein expression levels were measured after 8 weeks of intervention. Liquid intake in glucose- or sucrose-fed mice was about 2-fold compared with that in fructose-fed mice. The wild-type mice given glucose showed the highest total caloric intake and weight gain compared to the other groups. The serum concentrations of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and alanine transaminase (ALT) were significantly lowered in fat-1 groups compared with their paired wild-type groups. Histological analysis showed that the wild-type groups fed the HFS diets developed hepatic lipid accumulation and steatosis, compared with the fat-1 groups. The gene and protein expression levels involved in fatty acid synthesis and the toll-like receptor (TLR)-4 signaling pathway were significantly inhibited in the fat-1 groups compared with the wild-type groups. The endogenously synthesized n-3 PUFAs of the three fat-1 groups, which inhibit fatty acid synthesis and the TLR-4 signaling pathway, prevent HFS diet-induced NAFLD.

Development of an experimental diet model in rats to study hyperlipidemia and insulin resistance, markers for coronary heart disease.

Objectives:The objective of this study is to develop an experimental model of hyperlipidemia and insulin resistance (IR), markers of coronary heart disease (CHD) using high fat and high sugar (HFHS) diet and to evaluate the efficacy of the model using atorvastatin, a known antihyperlipidemic drug, pioglitazone, a known insulin sensitizer, and Tinospora cordifolia (Tc), an antidiabetic plant.Materials and Methods:Following Institutional Animal Ethics Committee permission, the study was conducted in male Wistar rats (200-270 g). The model was developed using a high fat (vanaspati ghee: coconut oil, 3:1) oral diet along with 25% fructose (high sugar) added in drinking water over a period of 6 weeks. Atorvastatin (2.1 mg/kg/day), pioglitazone (2.7 mg/kg/day) and Tc (200 mg/kg/day) were administered 3 weeks after initiation of HFHS diet and continued for another 3 weeks. Parameters assessed were weight, lipid profile, fasting blood glucose, insulin, and gastric emptying. Serum malondialdehyde (MDA) and catalase were assessed as markers of oxidative stress.Results:Administration of HFHS diet demonstrated a significant increase in blood glucose, insulin, total and low density lipoprotein cholesterol and triglycerides with a decrease in high density lipoprotein cholesterol. Treatment with test drugs decreased blood sugar, insulin, lipid parameters, increased gastric emptying rate, decreased MDA levels, and catalase activity when compared to HFHS diet group, confirming the efficacy of the model. Atherogenic index of all the test drugs (0.48, 0.57, and 0.53) was significantly lower as compared to HFHS diet group (1.107).Conclusion:This study confirms the development of a diet based cost-effective and time efficient experimental model, which can be used to study two important markers of cardiovascular disease that is, hyperlipidemia and IR and to explore the efficacy of new molecules in CHD.

The Effect of Intermittent Hypoxia on Bodyweight, Serum Glucose and Cholesterol in Obesity Mice

This article tests mice's indicators of body nutritional metabolism under tolerable hypoxic conditions, in order to explore the effects of moderate intermittent hypoxia on the bodyweight, blood sugar and blood cholesterol of obese mice and to identify the role of leptin in these effects; this study applies high-fat diet to establish Mice Obesity Models and observes the intervention effects of intermittent hypoxic training in this Model. Small healthy mice are classified in 4 groups at random, that is, Group A (Normal), Group B (Normal Hypoxia) fed with normal foods and undergoing Intermittent Hypoxic Training (IHT), Group C (Fatty-diet) fed with High-Fat and High-Sugar (HFHS) foods without IHT and Group D (Fatty-diet and Hypoxia) fed with HFHS foods with IHT. After 40 days of feeding and hypoxic training, weigh the mice, measure the levels of blood sugar and blood cholesterol with a full automatic biochemical analyzer, measure serum leptin concentration by enzyme-linked immunosorbent assay (ELISA) technique, inspect liver leptin receptor expression and liver fat slice by immunohistochemistry. It is found that compared to control group, after experiment, the average bodyweight, blood sugar, blood cholesterol and serum leptin concentration in Group C is increased significantly and numerous fat cells are distributed in the liver, which indicates that hyperlipemia model has been successfully established; after intermittent hypoxic training, the average bodyweight, blood sugar, blood cholesterol and liver fat cells distribution density and scope in Group B and D are lower than those in Group A and C, while serum leptin concentration is increased significantly; liver leptin receptor expression in Group D is higher than that in Group C. And hypoxia groups have no trauma conclusion. Moderate intermittent hypoxia can reduce bodyweight by increasing leptin concentration and enhancing liver leptin expression and it can also reduce the level of blood sugar and blood cholesterol and meanwhile prevent steatosis in liver cells effectively.