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This randomized controlled-feeding trial aimed to determine the impact of fried meat intake on the gut microbiota and fecal cometabolites and whether such impacts influenced host glucose homoeostasis, intestinal endotoxin levels, and systemic inflammation. RESEARCH DESIGN AND METHODSA total of 117 overweight adults were randomized into two groups. Fifty-nine participants were provided fried meat four times per week, and 58 participants were restricted from fried meat intake, while holding food group and nutrient compositions constant, for 4 weeks. The gut microbiota was analyzed by 16S rRNA sequencing. Glucose and insulin concentrations at 0, 30, 60, and 120 min of an oral glucose tolerance test, fecal microbiota-host cometabolite levels, and intestinal endotoxin and inflammation serum biomarker levels were measured. The area under the curve (AUC) for insulin, insulinogenic index (IGI), and muscle insulin resistance index (MIRI) were calculated. RESULTSThe participants who consumed fried meat had lower IGI values than the control subjects, but they had higher MIRI and AUC values of insulin and lipopolysaccharide (LPS), TNF-a, IL-10, and IL-1β levels (P < 0.05). Fried meat intake lowered microbial community richness and decreased Lachnospiraceae and Flavonifractor abundances while increasing Dialister, Dorea, and Veillonella abundances (P FDR <0.05), provoking a significant shift in the fecal cometabolite profile, with lower 3-indolepropionic acid, valeric acid, and butyric acid concentrations and higher carnitine and methylglutaric acid concentrations (P FDR <0.05). Changes in these cometabolite levels were significantly associated with changes in IGI and MIRI values and LPS, FGF21, TNF-a, IL-1β, and IL-10 levels (P < 0.05). CONCLUSIONSFried meat intake impaired glucose homoeostasis and increased intestinal endotoxin and systemic inflammation levels by influencing the gut microbiota and microbial-host cometabolites.

Prenatal malnutrition could promote renal dysfunction in adulthood, but it is unclear whether the detrimental effect could be transmitted to the next generation. We investigated whether famine exposure was associated with variation of estimated glomerular filtration rate(eGFR) in two generations and explored the mediation role of methylation alterations. The longitudinal analysis included 2909 participants from Suihua rural area. F1 and F2 generations were divided into non-famine and famine group based on their birth year and exposure status of their parents, respectively. The eGFR was calculated by using the chronic kidney disease epidemiology collaboration equation. We applied mixed-effect models to investigate the association between famine and ΔeGFR and tested blood DNA methylomes in 46 families across two generations. The mediation-analysis models were utilized to examine the mediation effect of methylation alterations on the famine-ΔeGFR association. In mixed-effect models, famine exposure was associated with declined ΔeGFR level in F1 (β:-8.32;95%CI:-11.51,-5.12) and in F2 (β:-6.11;95%CI:-11.88,-0.43). Methylation850K BeadChip data showed only 19 of 961 F1 differentially methylated sites showed concordant alterations in F2. The mediation-analysis results showed methylation alterations on AGTR1 and PRKCA might mediate the famine-ΔeGFR association. Overall, prenatal famine exposure may have long-term effects on eGFR decline across consecutive generations which might be partly mediated by methylation alterations on AGTR1 and PRKCA.

Context Emerging evidence suggests that not only the quantity but also the quality and food sources of macronutrients plays an important role in CVD. However, limited studies have examined the association of meal timing of different quality of macronutrients with CVD risk. Objective This study aimed to examine the association of subtypes of macronutrient consumption at dinner vs breakfast with cardiovascular diseases (CVD). Methods A total of 27 911 participants from the National Health and Nutrition Examination Survey (2003-2016) were included. The differences of subtypes of macronutrients at dinner vs breakfast (Δratio) were categorized into quintiles. Multiple logistic regression models and isocaloric substitution effects of subtypes were performed. Results After adjustment of a variety of covariates, participants in the highest quintile of the Δratio of low-quality carbohydrates had a higher risk of angina (odds ratio [OR] = 1.63; 95% CI, 1.16-2.29) (Pfor trend = .007) and heart attack (OR = 1.47; 95% CI, 1.13-1.93) (Pfor trend = .068) compared with the lowest quintile. The highest quintile of the Δratio of animal protein had a higher risk of coronary heart disease (OR = 1.44; 95% CI, 1.06-1.95) (Pfor trend = .014) and angina (OR = 1.44; 95% CI, 1.01-2.07) (Pfor trend = .047). For the Δratio of unsaturated fatty acid (USFA), the highest quintile of the Δratio of USFA was related to lower stroke risk (OR = 0.76; 95% CI, 0.58-0.99) (Pfor trend = .049). Isocaloric substitution of low-quality carbohydrates/animal protein by high-quality carbohydrates/plant protein at dinner reduced CVD risk by around 10%. Conclusion This study indicated that overconsumption of low-quality carbohydrates and animal protein at dinner rather than breakfast was significantly associated with higher CVD risk and USFA consumption at dinner related to lower CVD risk among US adults. Substitution of low-quality carbohydrates or animal protein by high-quality carbohydrates or plant protein at dinner could reduce CVD risk.

The imidazoline I-1 receptor (I-1 R) agonists are widely used to lower blood pressure, but their effects on hyperlipidemia are still obscure. The present study is aimed to evaluate the possible mechanism(s) of I-1 R in the regulation of lipid homeostasis. Farnesoid X receptor (FXR) plays an important role in blood lipid homeostasis; however, the role of FXR in rilmenidine-induced blood lipid lowering action is still unknown. Thus, we administered rilmenidine, a selective agonist of I-1 R, into high fat diet-fed (HFD) mice showing hypertriglyceridemia and hypercholesterolemia. Rilmenidine significantly ameliorated hyperlipidemia in HFD mice after 7 days of administration. Pretreatment with efaroxan, at a dose sufficient to inhibit I-1 R activation, blocked the effects of rilmenidine. Also, in cultured HepG2 cells, rilmenidine dose-dependently induced the expression of farnesoid X receptor (FXR). The rilmenidine-induced FXR expression and FXR-related genes were blocked by efaroxan. However, rilmenidine treatment did not affect the expression of enzymes related to β-oxidation. In conclusion, activation of I-1 R may activate FXR to lower plasma lipids, suggesting I-1 R as a new target for the treatment of hyperlipidemia.

BackgroundCurrent studies on the protective effects of dietary spermidine (SPD) on cardiovascular disease (CVD) are mainly limited to animal studies, and the relationship between dietary SPD and CVD mortality remains inconclusive.ObjectiveThis study aims to evaluate the association between dietary SPD intake and CVD and all-cause mortality.MethodsA total of 23,894 people enrolled in the National Health and Nutrition Examination Survey (NHANES) from 2003 to 2014 were recruited for this study. The dietary intake of SPD from 11 specific food origins and total SPD was categorized into tertiles or quartiles. Cox proportional hazard regression models were developed to evaluate the association of SPD intake with CVD and all-cause mortalities.ResultsAmong the 23,894 participants, 2,365 deaths, including 736 deaths due to CVD, were documented. After adjustment for potential confounders, compared with participants in the lowest quartile, participants in the highest quartile of total SPD had a significantly lower risk of CVD mortality (HR = 0.68, 95% CI: 0.51–0.91) and all-cause mortality (HR = 0.70, 95% CI: 0.60–0.82); participants in the highest tertiles or quartiles of vegetable-derived SPD, cereal-derived SPD, legume-derived SPD, nut-derived SPD, and cheese-derived SPD had a lower risk of CVD mortality (HR vegetable − derivedSPD = 0.68, 95% CI: 0.54–0.86; HR cereal − derivedSPD = 0.75, 95% CI: 0.57–0.97; HR legume − derivedSPD = 0.68, 95% CI: 0.52–0.88; HR nut − derivedSPD = 0.66, 95% CI: 0.53–0.80; HR cheese − derivedSPD = 0.68, 95% CI: 0.52–0.88) and all-cause mortality (HR vegetable − derivedSPD = 0.73, 95% CI: 0.64–0.84; HR cereal − derivedSPD = 0.80, 95% CI: 0.69–0.93; HR legume − derivedSPD = 0.70, 95% CI: 0.60–0.80;HR nut − derivedSPD = 0.72, 95% CI: 0.64–0.81; HR cheese − derivedSPD = 0.70, 95% CI: 0.61–0.81) than those in the lowest tertiles or quartiles. Moreover, subgroup analysis showed consistent associations among the people with hypertension and hyperlipidemia.ConclusionHigher intake of dietary SPD is associated with decreased risk of CVD and all-cause mortality, and among specific food origin SPD, SPD derived from vegetables, cereals, legumes, nuts, and cheese was associated with reduced CVD and all-cause mortality.

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