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Hepatic steatosis can occur in lean individuals, while its metabolic and risk profiles remain unclear. We aimed to characterize the clinical and risk profiles of lean and non-lean steatosis. This cross-sectional study included 1610 patients with transient elastography-assessed steatosis. The metabolic and risk profiles were compared. Compared to their non-lean counterparts, lean subjects with steatosis had a lower degree of fibrosis (F0–F1: 91.9% vs. 80.9%), had a lower prevalence of diabetes (27.9% vs. 32.8%), dyslipidemia (54.7% vs. 60.2%) and hypertension (50.0% vs. 51.3%), and had higher levels of high-density lipoprotein cholesterol while lower fasting insulin and homeostatic model assessment for insulin resistance (all p < 0.05). Of the 16 potential risk factors, being Hispanic was associated with higher odds of non-lean steatosis but not with lean steatosis (odds ratio (OR): 2.07 vs. 0.93), while excessive alcohol consumption had a different trend in the ratio (OR: 1.47 vs.6.65). Higher waist-to-hip ratio (OR: 7.48 vs. 2.45), and higher waist circumference (OR: 1.14 vs. 1.07) showed a stronger positive association with lean steatosis than with non-lean steatosis (all Pheterogeneity < 0.05). Although lean individuals with steatosis presented a healthier metabolic profile, both lean and non-lean steatosis had a significant proportion of metabolic derangements. In addition, the etiological heterogeneity between lean and non-lean steatosis may exist. [ABSTRACT FROM AUTHOR]

Epidemiological research has demonstrated that the increase in high fat consumption has promoted the morbidity of diabetes. Exposure to organophosphorus pesticides (such as chlorpyrifos) may also increase the risk of diabetes. Although chlorpyrifos is a frequently detected organophosphorus pesticide, the interaction effect between chlorpyrifos exposure and a high-fat diet on glucose metabolism is still unclear. Thus, the effects of chlorpyrifos exposure on glucose metabolism in rats eating a normal-fat diet or a high-fat diet were investigated. The results demonstrated that the glycogen content in the liver decreased and that the glucose content increased in chlorpyrifos-treated groups. Remarkably, the ATP consumption in the chlorpyrifos-treatment group was promoted in the rats eating a high-fat diet. However, chlorpyrifos treatment did not change the serum levels of insulin and glucagon. Notably, the contents of liver ALT and AST changed more significantly in the high-fat chlorpyrifos-exposed group than in the normal-fat chlorpyrifos-exposed group. Chlorpyrifos exposure caused an increase in the liver MDA level and a decrease in the enzyme activities of GSH-Px, CAT, and SOD, and the changes were more significant in the high-fat chlorpyrifos-treatment group. The results indicated that chlorpyrifos exposure led to disordered glucose metabolism in all dietary patterns as a result of antioxidant damage in the liver, in which a high-fat diet may have aggravated its toxicity. [ABSTRACT FROM AUTHOR]

Sulforaphane (SFN) was generated by the hydrolysis of glucoraphanin under the action of myrosinase. However, due to the instability of SFN, the bioavailability of SFN was limited. Meanwhile, the gut flora obtained the ability to synthesize myrosinase and glucoraphanin, which could be converted into SFN in the intestine. However, the ability of microorganisms to synthesize myrosinase in the gut was limited. Therefore, microorganisms with myrosinase synthesis ability need to be supplemented. With the development of research, microorganisms with high levels of myrosinase synthesis could be obtained by artificial selection and gene modification. Researchers found the SFN production rate of the transformed microorganisms could be significantly improved. However, despite applying transformation technology and regulating nutrients to microorganisms, it still could not provide the best efficiency during generating SFN and could not accomplish colonization in the intestine. Due to the great effect of microencapsulation on improving the colonization ability of microorganisms, microencapsulation is currently an important way to deliver microorganisms into the gut. This article mainly analyzed the possibility of obtaining SFN-producing microorganisms through gene modification and delivering them to the gut via microencapsulation to improve the utilization rate of SFN. It could provide a theoretical basis for expanding the application scope of SFN. [ABSTRACT FROM AUTHOR]

There is little evidence for the associations of the overall plant-based diet index (PDI), the healthful PDI (hPDI), and the unhealthful PDI (uPDI) with the odds of nonalcoholic fatty liver disease (NAFLD). We present a nationwide cross-sectional study among US adults aged 18 years or older. Diet was assessed by 24-h recalls. Overall PDI, hPDI, and uPDI were constructed based on 18 food groups. NAFLD was defined based on controlled attenuation parameter derived via transient elastography (TE) in the absence of other causes of chronic liver disease. Among 3900 participants with eligible TE examination, 1686 were diagnosed with NAFLD. The overall PDI was not associated with NAFLD prevalence (comparing extreme tertiles of PDI score OR = 1.03, 95% CI 0.76, 1.38, ptrend = 0.609). However, hPDI was inversely (OR = 0.50, 95% CI 0.35, 0.72, ptrend < 0.001), while uPDI was positively associated with odds of NAFLD (OR = 1.37, 95% CI 0.93, 2.02, ptrend = 0.009) in the multivariable-adjusted models without body mass index (BMI). After further adjustment for BMI, only the association of hPDI with NAFLD remained statistically significant (OR = 0.64, 95% CI 0.46, 0.87, ptrend = 0.006). Such inverse association appeared stronger in non-Hispanic whites, but not in other racial/ethnic groups (pinteraction = 0.009). Our findings suggest that a plant-based diet rich in healthy plant foods might be associated with lower odds of NAFLD, particularly among US non-Hispanic whites. Clinical trials and cohort studies to validate our findings are needed. [ABSTRACT FROM AUTHOR]

Background: Acrylamide is formed during food heating and is neurotoxic to animals and potentially carcinogenic to humans. It is important to reduce acrylamide content during food processing. Researchers have suggested that garlic powder could reduce acrylamide content, but the key substance and acrylamide reduction pathway of garlic powder was unclear. Methods: The inhibitory effect of garlic powder on acrylamide in asparagine/glucose solution and a fried potato model system were firstly evaluated. Furthermore, the effect of allicin on the amount of produced acrylamide in the asparagine/glucose solution model system and fried potatoes was studied with kinetic analysis. Results: The freeze-dried garlic powder had a higher inhibition rate (41.0%) than oven-dried garlic powder (maximum inhibition rate was 37.3%), and allicin had a 71.3% attribution to the reduction of acrylamide content. Moreover, the inhibition rate of allicin had a nonlinear relationship with the addition level increase. The kinetic analysis indicated that garlic powder and allicin could reduce acrylamide content through the AA formation stage, but not the decomposition stage. Conclusions: Allicin was the key component of garlic powder in reducing acrylamide content during acrylamide formation stage. This research could provide a new method to reduce acrylamide content during food processing and expand the application area of garlic. [ABSTRACT FROM AUTHOR]

There is little evidence for the association between fruit juice, especially 100% fruit juice, and mortality risk. In addition, whether 100% fruit juice can be a healthy alternative to whole fruit remains uncertain. This prospective study utilized the data from the US National Health and Nutrition Examination Survey (NHANES) from 1999 to 2014. After a median follow-up of 7.8 years, 4904 deaths among 40,074 participants aged 18 years or older were documented. Compared to non-consumption, daily consumption of 250 g or more of 100% fruit juice was associated with higher overall mortality (hazard ratio (HR) = 1.30, 95% confidence interval (CI): 1.11–1.52) and mortality from heart disease (HR = 1.49, 95 CI: 1.01–2.21). A similar pattern was observed for total fruit juice, with HRs of 1.28 (95% CI: 1.09–1.49) for overall mortality and 1.48 (95% CI: 1.01–2.17) for heart disease mortality. Replacing 5% of energy from whole fruit with 100% or total fruit juice was associated with a 9% (95% CI: 2–16%) and 8% (95% CI: 1–15%) increased mortality risk, respectively. Our findings suggest that both total and 100% fruit juice could be associated with high mortality risk, and need to be validated in well-designed studies given the potential misclassification of diet and death reasons. [ABSTRACT FROM AUTHOR]