Nutrition & Metabolism最新文献

Purpose: This study aims to investigate the association of serum TSH with BMD in Chinese adults with normal thyroid function.

Methods: These participants were divided into tertiles based on serum TSH levels. Linear regression model and multinomial logistic regression models were used to analyze the associations of continuous BMD and categorical BMD with serum TSH, respectively.

Results: In women younger than 60 years, BMD decreased with the increase of TSH at normal level, while in women older than 60 years, BMD increased with the increase of TSH at normal level; besides, the BMD of women younger than 60 years old was significantly higher than that of women over 60 years old (156.05 ± 39.34 mg/cm³ vs. 86.95 ± 29.51 mg/cm³, P < 0.001). Linear regression results showed negative associations of BMD and normal TSH level in women with age younger than 60 years (β=-4.34, P < 0.001), but this inverse trend was observed in women over 60 years old (β = 2.04, P = 0.041). Both in men younger than 60 years and over 60 years old, BMD decreased with the increase of TSH at normal levels; besides, the BMD of men younger than 60 years was significantly higher than those over 60 years old (143.08 ± 32.76 mg/cm³ vs. 108.13 ± 31.99 mg/cm³, P < 0.001).

Conclusions: The results demonstrated an opposite trend in BMD at normal TSH levels in younger and elder females, that is, in females younger than 60 years, BMD decreased with the increase of TSH, which indicated that TSH might play a different role in younger and elder females. However, this trend was not significant in males.

Background: No research report has been conducted to investigate the impact of oxidation balance score (OBS) on the estimated pulse wave velocity(ePWV).We aimed to examine the association between OBS and ePWV.

Method: We evaluated data for 13,073 patients from the National Health and Nutrition Examination Survey (NHANES). The exposure variable was OBS. The outcome variables was combination of ePWV and arterial stiffness.

Results: We observed a significant negative correlation between OBS (Per 1SD increase) and ePWV in the gradually adjusted models. Based on the aforementioned results, a two-piecewise logistic regression adjusted model was subsequently employed to establish the association between OBS and elevated ePWV, and the inflection point was determined as 5. The increased risk of elevated ePWV (OR:0.70; 95%CI:0.51-0.94) gradually decreases with the increase of OBS on the left side of the inflection point; however, when OBS exceeds 5, this decrease in risk of elevated ePWV(OR:1.00; 95%CI:0.96-1.04) is no longer observed (P for log likelihood ratio test = 0.028).

Conclusions: There exists a significant association between OBS and ePWV in the context of American adults. Specifically, OBS exhibits a negative correlation with ePWV; however, when considering an elevated ePWV, a saturation effect is observed in relation to OBS.

Background: Obesity and its associated complications raise significant public concern, revealing gender disparities in the susceptibility to metabolic disorders, with females often displaying greater resistance to obesity-related metabolic disorder than males. Sestrin2 is a crucial protein involved in metabolism and energy balance. This study seeks to explore whether Sesn2 knockout (KO) exacerbates high-fat diet (HFD) induced obesity in female mice.

Methods: Female mice with wild-type (WT) and Sesn2 KO were subjected to a 12-week regimen of normal diet or HFD. Using a Body Composition Analyzer, body composition was gauged. Biochemical assays encompassed glucose, lipid, and liver function measurements, alongside 24-hour urine albumin excretion. Echocardiographic evaluation assessed cardiac function. Histopathological analysis of key metabolic tissues (liver, kidney, and heart tissues) were conducted. Western blotting or qRT-PCR evaluated key proteins and genes linked to inflammation, mitochondrial, and lipid metabolism in adipose tissues.

Results: In comparison to mice fed a regular diet, those on a HFD exhibited significant increases in body weight and fat mass. Notably, Sesn2 KO further aggravated obesity, showcasing the most pronounced metabolic anomalies: elevated body weight, fat mass, impaired glucose tolerance, and insulin sensitivity, alongside heightened levels of free fatty acids and triglycerides. Additionally, KO-HFD mice displayed exacerbated multi-tissue impairments, including elevated hepatic enzymes, increased urinary albumin excretion, compromised cardiac function, and accumulation of lipids in the liver, kidney, and heart. Moreover, adipose tissue showcased altered lipid dynamics and function, characterized by enhanced triglyceride breakdown and modified adipokine levels. Browning was diminished, along with decreased Pgc1α and Sirt1 in KO-HFD mice.

Conclusion: Sesn2 KO exacerbates HFD-induced obesity and metabolic disorders in female mice. These findings underscore Sestrin2's novel role as a regulator of obesity in female mice.

Background: This prospective cohort study aimed to investigate the association between ultra-processed food (UPF) and the risk of metabolic syndrome (MetS), as well as to assess whether fruit and vegetable intake and weight change modify this association.

Methods: We included 1915 healthy participants who participated in the Tehran Lipid and Glucose Study (TLGS), all of whom had complete demographic, anthropometric, and dietary measurements. A validated food frequency questionnaire was used to assess UPF consumption based on the NOVA classification system. MetS was defined according to the Joint Interim Statement. Multivariable adjusted Cox regression was used to estimate hazard ratios (HRs) for MetS events across tertiles of UPF. The effect of fruit and vegetable consumption and weight change on this association was assessed using joint classification by Cox regression.

Results: UFP consumption showed no association with MetS risk after adjusting for confounders. However, after adjustment for dietary fiber, fruits, and vegetables, the highest tertile of UPF consumption was positively linked to MetS risk, compared to the lowest tertile. There was a significant interaction between fruit, vegetable, and dietary fiber intake and UPF consumption concerning the risk of MetS (All P values < 0.05). Among individuals consuming less than 248 g/day of fruit, the risk of MetS increased by 54% (confidence interval: 1.13-2.10) in the highest UPF tertile. Consuming vegetables and dietary fiber below the median (258 g/day and 42.2 g/day, respectively) increased the risk of MetS in the third tertile of UPF. However, consuming vegetables and fiber ≥ median intake, reduced the risk of MetS among those with the lowest UPF consumption. Furthermore, the risk of MetS was observed in the third tertile of UPF consumption among individuals with fruit and vegetable consumption < 537 g/day. UPF consumption was not associated with the risk of MetS in different weight change statuses.

Conclusions: Consuming more fruits and vegetables mitigated the adverse effect of UPF on the risk of developing MetS.

Background: The pathogenesis of diabetic cardiomyopathy is closely linked to abnormal glycosylation modifications. N-acetylglucosaminyltransferase V (GnT-V), which catalyzes the production of N-linked -1-6 branching of oligosaccharides, is involved in several pathophysiological mechanisms of many disorders, including cardiac hypertrophy and heart failure. However, the mechanism by which GnT-V regulates cardiac hypertrophy in diabetic cardiomyopathy is currently poorly understood. In this study, we investigated the role of GnT-V on myocardial hypertrophy in diabetic cardiomyopathy and elucidated the underlying mechanisms.

Material and methods: Streptozotocin (STZ) was intraperitoneally injected into mice to induce diabetic cardiomyopathy. An adeno-associated virus (AAV) carrying negative control small hairpin RNA (shNC) or GnT-V-specifc small hairpin RNA (shGnT-V) was used to manipulate GnT-V expression. In our study, forty male C57BL/6J mice were randomly divided into four groups (10 mice per group): control mice with AAV-shNC, diabetic cardiomyopathy mice with AAV-shNC, control mice with AAV-shGnT-V, and diabetic cardiomyopathy mice with AAV-shGnT-V. In addition, H9C2 cells and primary neonatal cardiac fibroblasts treated with high glucose were used as a cell model of diabetes. Analysis of cardiac hypertrophy and fibrosis, as well as functional studies, were used to investigate the underlying molecular pathways.

Results: AAV-mediated GnT-V silencing dramatically improved cardiac function and alleviated myocardial hypertrophy and fibrosis in diabetic mice. In vitro experiments demonstrated that GnT-V was elevated in cardiomyocytes and induced cardiomyocyte hypertrophy in response to high glucose stimulation. GnT-V knockdown significantly reduced the expression of the integrinβ1 signaling pathway, as evidenced by decreased downstream ERK1/2 activity, which inhibited cardiomyocyte hypertrophy accompanied by reduced ANP, BNP, and β-MHC expression. Furthermore, knocking down GnT-V expression lowered the TGF-β1-Smads signaling pathway, which reduced the expression of α-SMA, collagen I, and collagen III.

Conclusions: Overall, our research indicated that GnT-V may be a useful therapeutic target to treat diabetic cardiomyopathy, primarily in the inhibition of myocardial hypertrophy and fibrosis.

Background: The association of BCAAs (isoleucine, leucine, and valine) with cardiovascular and cerebrovascular diseases has been widely recognized by researchers, but there is limited evidence to support the relationship between BCAAs and multiple chronic conditions (MCCs) in older adults. This study aimed to explore the correlation between BCAA levels in the diets of older adults and MCCs.

Methods: Based on a health management cohort project in Nanshan District of Shenzhen, 4278 individuals over 65 years old were selected as participants via multi-stage stratified sampling from May 2018 to December 2019. Data were collected using a validated semi-quantitative food frequency questionnaire, as well as anthropometric and chronic disease reports. MCC was defined as the coexistence of two or more chronic diseases, namely, hypertension, dyslipidemia, diabetes, CAD, stroke, CKD, and CLD. Multivariate unconditional logistic regression analysis was used to analyze the relationship between dietary BCAAs and MCCs in older adults, and then, gender stratification analysis was performed. A restricted cubic spline model (a fitted smooth curve) was used to determine the dose-response relationship of isoleucine with MCCs.

Results: A total of 4278 older adults aged 65 and above were included in this study, with an average age of 72.73 ± 5.49 years. The cohort included 1861 males (43.50%). Regardless of whether confounding factors were corrected, isoleucine was a risk factor for MCCs (OR = 3.388, 95%CI:1.415,8.109). After gender stratification, the relationships between dietary isoleucine and MCCs (OR = 6.902, 95%CI:1.875,25.402) and between leucine (OR = 0.506,95%CI:0.309,0.830) and MCCs were significant in women, but not in men. No significant association between valine and MCCs was observed. In addition, isoleucine was a risk factor for MCCs when its intake was greater than 4.297 g/d.

Conclusion: Isoleucine may play an important role in regulating age-related diseases. BCAAs such as isoleucine can be used as risk markers for MCCs in older adults.

Purpose: Using data from the National Health and Nutrition Examination Survey (NHANES) and employing Controlled Attenuation Parameter (CAP) measures, this study explores the correlation between vitamin E (VE) intake and hepatic steatosis and its impact on different subsets.

Materials and methods: We selected 5757 participants with CAP data from the 2017-2020 NHANES dataset. Daily VE intake was assessed by a 24-hour dietary recall. Hepatic fat content was quantified using transient elastography to measure CAP. Stratified multivariable regression analysis investigated relationships in different subsets, and a generalized additive model identified nonlinear relationships and thresholds.

Results: After adjusting for confounders, higher VE intake correlated with lower CAP levels. Subgroup analyses and tests for interaction revealed a significantly stronger negative correlation between VE intake and CAP in obese individuals. Further analysis indicated a curvilinear relationship between VE intake and the severity of liver fat degeneration in both the general study population and the obese subgroup, demonstrating a threshold effect. In the general population, VE intake below the threshold (6.58 mg/day) is positively correlated with CAP levels, whereas intake above this threshold shows a negative correlation. For obese individuals, the threshold is set at 7.37 mg/day, above which the negative correlation with CAP is even more pronounced.

Conclusion: Our study revealed a negative correlation between VE intake and hepatic fat content, highlighting the potentially crucial role VE plays in obese fatty liver patients. Importantly, we identified threshold effects of VE intake in both general and obese populations. Our results support clinical nutritional interventions, personalized dietary guidance, and the development of drugs to combat fatty liver.

Background: Cardiovascular disease (CVD) is a chronic disease with a serious prognosis, and obesity is a risk factor for CVD. Lipid accumulation product index (LAP) is a new indicator of obesity, waist circumference, and triglycerides were included in the formula, but its association with CVD is inconsistent. Therefore, this study researched the effect of LAP levels on CVD.

Methods: This prospective cohort study was based on the Kailuan cohort. A total of 95,981 participants who completed the first physical examination in 2006 and had no history of CVD or LAP absence were included. The participants were divided into four groups according to the LAP quartile (Q1 - Q4). Up until December 31, 2022, incidence density was calculated for each group. The hazard ratio (HR) and 95% confidence interval (CI) of CVD in each group were calculated by the Cox proportional hazards model.

Results: During a median follow-up period of 15.95 years, 9925 incident CVD events occurred (2123 myocardial infarction and 8096 stroke). There were differences in potential confounders among the four groups (P < 0.001). The incidence density and 95% CI of CVD in Q1-Q4 groups were 4.76(4.54, 5.00), 6 0.50(6.24, 6.77), 8.13(7.84, 8.44) and 9.34(9.02, 9.67), respectively. There were significant differences in the survival curves among the four groups by log-rank test (P < 0.001). After adjusting for potential confounders, Cox proportional hazards model results showed that compared with the Q1 group, the HR and 95% CI of CVD in the Q2, Q3, and Q4 groups were1.15(1.08, 1.23), 1.29(1.21, 1.38) and 1.39(1.30, 1.49), respectively. The HR and 95%CI of myocardial infarction were 1.28(1.10, 1.49), 1.71(1.47, 1.98) and 1.92(1.64, 2.23), respectively. The HR and 95%CI of stroke were 1.11 (1.03, 1.19), 1.20 (1.12, 1.29) and 1.28 (1.19, 1.38), respectively. After subgroup analysis by gender, there was no significant interaction (P = 0.169), and the relationship between LAP and CVD in different genders was consistent with the main results. After subgroup analysis by age, there was a significant interaction (P = 0.007), and the association between LAP and CVD in different age groups was consistent with the main results. After subgroup analysis by BMI, there was no significant interaction (P = 0.506), and the association between LAP and CVD in different BMI groups was consistent with the main results. The results remained robust after sensitivity analyses. For each unit increase in ln(LAP), the HR and 95%CI of CVD were 4.07 (3.92, 4.23).

Conclusion: This study demonstrated that the risk of CVD increased with the increase of LAP level. The risk of CVD in group Q2 - Q4 was 1.15, 1.29, and 1.39 times higher than that in group Q1, respectively.

Clinical trial registration number: ChiCTR2000029767.

Background: Cardiovascular disease (CVD) affects millions worldwide and is the leading cause of death among non-communicable diseases. Western diets typically comprise of meat and dairy products, both of which are rich in cholesterol (Cho) and methionine (Met), two well-known compounds with atherogenic capabilities. Despite their individual effects, literature on a dietary combination of the two in the context of CVD are limited. Therefore, studies on the combined effects of Cho and Met were carried out using male Sprague Dawley rats. An additional interest was to investigate the cardioprotective potential of sitagliptin, an anti-type 2 diabetic drug. We hypothesized that feeding a dietary combination of Cho and Met would result in adverse cardiac effects and would be attenuated upon administration of sitagliptin.

Methods: Adult male Sprague-Dawley rats were fed either a control (Con), high Met (1.5%), high Cho (2.0%), or high Met (1.5%) + high Cho (2.0%) diet for 35 days. They were orally gavaged with an aqueous preparation of sitagliptin (100 mg/kg/d) or vehicle (water) from day 10 through 35. On day 36, rats were euthanized, and tissues were collected for analysis.

Results: Histopathological evaluation revealed a reduction in myocardial striations and increased collagen deposition in hypercholesterolemia (HChol), responses that became exacerbated upon sitagliptin administration. Cardiac pro-inflammatory and pro-fibrotic responses were adversely impacted in similar fashion. The addition of Met to Cho (MC) attenuated all adverse structural and biochemical responses, with or without sitagliptin.

Conclusions: Adverse cardiac outcomes in HChol were enhanced by the administration of sitagliptin, and such effects were alleviated by Met. Our findings could be significant for understanding or revisiting the risk-benefit evaluation of sitagliptin in type 2 diabetics, and especially those who are known to consume atherogenic diets.