Dietary sugars: their detection by the gut-brain axis and their peripheral and central effects in health and diseases.

BACKGROUND: Substantial increases in dietary sugar intake together with the increasing prevalence of obesity worldwide, as well as the parallels found between sugar overconsumption and drug abuse, have motivated research on the adverse effects of sugars on health and eating behaviour. Given that the gut-brain axis depends on multiple interactions between peripheral and central signals, and because these signals are interdependent, it is crucial to have a holistic view about dietary sugar effects on health. METHODS: Recent data on the effects of dietary sugars (i.e. sucrose, glucose, and fructose) at both peripheral and central levels and their interactions will be critically discussed in order to improve our understanding of the effects of sugars on health and diseases. This will contribute to the development of more efficient strategies for the prevention and treatment for obesity and associated co-morbidities. RESULTS: This review highlights opposing effects of glucose and fructose on metabolism and eating behaviour. Peripheral glucose and fructose sensing may influence eating behaviour by sweet-tasting mechanisms in the mouth and gut, and by glucose-sensing mechanisms in the gut. Glucose may impact brain reward regions and eating behaviour directly by crossing the blood-brain barrier, and indirectly by peripheral neural input and by oral and intestinal sweet taste/sugar-sensing mechanisms, whereas those promoted by fructose orally ingested seem to rely only on these indirect mechanisms. CONCLUSIONS: Given the discrepancies between studies regarding the metabolic effects of sugars, more studies using physiological experimental conditions and in animal models closer to humans are needed. Additional studies directly comparing the effects of sucrose, glucose, and fructose should be performed to elucidate possible differences between these sugars on the reward circuitry.

Impacts of child sexual abuse: The mediating role of future orientation on academic outcomes.

BACKGROUND: Child Sexual Abuse (CSA) has significant impacts on an individual's physical and mental well-being including substance use, depression, anxiety, post-traumatic stress disorder, relationship issues, as well as sexual revictimization in adulthood. Positive future orientation is associated with higher educational outcomes and successful goal attainment, but CSA survivors have lower educational attainment and less employment opportunities leading to less financial security in adulthood. OBJECTIVE: Our study seeks to examine whether future orientation mediates the relationship between CSA and academic outcomes using data from the Kaplan Longitudinal and Multigenerational Study (KLAMS). PARTICIPANTS & SETTING: KLAMS is a U.S. based panel study which captures information about the mental health, relationships, academic outcomes, and deviant behavior of two generations of family members at multiple points in time. In the present study, we use data from two separate interviews with the children (N = 2084) of the original respondents. METHODS: We estimated a series of regressions using generalized structural equation modeling to examine the relationship between child sexual abuse, future orientation, and three different types of academic outcomes. RESULTS: Youth who experienced sexual abuse had lower grades in school, were more likely to drop out, and had lower levels of education than children with no history of sexual abuse. Negative future orientation mediated the relationship between child sexual abuse and all three outcomes. CONCLUSIONS: In support of existing research, we found child sexual abuse has a negative impact on positive future orientation, and positive future orientation contributes to better academic outcomes.

Effects of Chronic Consumption of Sugar-Enriched Diets on Brain Metabolism and Insulin Sensitivity in Adult Yucatan Minipigs.

Excessive sugar intake might increase the risk to develop eating disorders via an altered reward circuitry, but it remains unknown whether different sugar sources induce different neural effects and whether these effects are dependent from body weight. Therefore, we compared the effects of three high-fat and isocaloric diets varying only in their carbohydrate sources on brain activity of reward-related regions, and assessed whether brain activity is dependent on insulin sensitivity. Twenty-four minipigs underwent 18FDG PET brain imaging following 7-month intake of high-fat diets of which 20% in dry matter weight (36.3% of metabolisable energy) was provided by starch, glucose or fructose (n = 8 per diet). Animals were then subjected to a euglycemic hyperinsulinemic clamp to determine peripheral insulin sensitivity. After a 7-month diet treatment, all groups had substantial increases in body weight (from 36.02±0.85 to 63.33±0.81 kg; P<0.0001), regardless of the diet. All groups presented similar insulin sensitivity index (ISI = 1.39±0.10 mL·min-1·µUI·kg). Compared to starch, chronic exposure to fructose and glucose induced bilateral brain activations, i.e. increased basal cerebral glucose metabolism, in several reward-related brain regions including the anterior and dorsolateral prefrontal cortex, the orbitofrontal cortex, the anterior cingulate cortex, the caudate and putamen. The lack of differences in insulin sensitivity index and body weight suggests that the observed differences in basal brain glucose metabolism are not related to differences in peripheral insulin sensitivity and weight gain. The differences in basal brain metabolism in reward-related brain areas suggest the onset of cerebral functional alterations induced by chronic consumption of dietary sugars. Further studies should explore the underlying mechanisms, such as the availability of intestinal and brain sugar transporter, or the appearance of addictive-like behavioral correlates of these brain functional characteristics.

Obesogenic diets have deleterious effects on fat deposits irrespective of the nature of dietary carbohydrates in a Yucatan minipig model.

The effects of digestible carbohydrates, fructose in particular, on the development of metabolic disturbances remain controversial. We explored the effects of prolonged consumption of high-fat diets differing in their carbohydrate source on fat deposits in the adult Yucatan minipig. Eighteen minipigs underwent computed tomographic imaging and blood sampling before and after 8 weeks of three isocaloric high-fat diets with different carbohydrate sources (20% by weight for starch in the control diet, glucose or fructose, n=6 per diet). Body adiposity, liver volume, and fat content were estimated from computed tomographic images (n=18). Liver volume and lipid content were also measured post mortem (n=12). We hypothesized that the quantity and the spatial distribution of fat deposits in the adipose tissue or in the liver would be altered by the nature of the carbohydrate present in the obesogenic diet. After 8 weeks of dietary exposure, body weight (from 26±4 to 58±3 kg), total body adiposity (from 38±1 to 47±1%; P<.0001), liver volume (from 1156±31 to 1486±66 mL; P<.0001), plasma insulin (from 10±1 to 14±2 mIU/L; P=.001), triacylglycerol (from 318±37 to 466±33 mg/L; P=.005), and free-fatty acids (from 196±60 to 396±59 µmol/L; P=.0001) increased irrespective of the carbohydrate type. Similarly, the carbohydrate type did not induce changes in the spatial repartition of the adipose tissue. Divergent results were obtained for fat deposits in the liver depending on the investigation method. In conclusion, obesogenic diets alter adipose tissue fat deposits and the metabolic profile independently of the nature of dietary carbohydrates.

Soy protein reduces hepatic lipotoxicity in hyperinsulinemic obese Zucker fa/fa rats.

Hepatic steatosis is commonly present during the development of insulin resistance, and it is a clear sign of lipotoxicity attributable in part to an accelerated lipogenesis. There is evidence that a soy protein diet prevents the overexpression of hepatic sterol-regulatory element binding protein-1 (SREBP-1), decreasing lipid accumulation. Therefore, the aim of the present work was to study whether a soy protein diet may prevent the development of fatty liver through the regulation of transcription factors involved in lipid metabolism in hyperinsulinemic and hyperleptinemic Zucker obese fa/fa rats. Serum and hepatic cholesterol and triglyceride levels, as well as VLDL-triglyceride and LDL-cholesterol, were significantly lower in rats fed soy protein than in rats fed a casein diet for 160 days. The reduction in hepatic cholesterol was associated with a low expression of liver X receptor-alpha and its target genes, 7-alpha hydroxylase and ABCA1. Soy protein also decreased the expression of SREBP-1 and several of its target genes, FAS, stearoyl-CoA desaturase-1, and delta5 and delta6 desaturases, decreasing lipogenesis even in the presence of hyperinsulinemia. Reduction in SREBP-1 was not associated with the presence of soy isoflavones. Finally, soy protein reduced SREBP-1 expression in adipocytes, preventing hypertrophy, which also helps prevent the development of hepatic lipotoxicity.