Nutrition & Diabetes最新文献

Objectives: Present report evaluates the protective effect of geraniol on high fat diet (HFD) induced obesity in rats and also determines the molecular mechanism of it.

Methods: Rats were induced with obesity with administration of HFD for four weeks and geraniol 200 and 400 mg/kg p.o. was administered for the next four week in the respective groups. Blood glucose and oral glucose tolerance test (OGTT), lipid profile was estimated in the geraniol treated HFD induced obesity in rats. Moreover, docking study was performed to determine the specific mechanism of geraniol by targeting HMG-CoE A reductase (in silico).

Results: There was significant increase in body weight and amelioration in altered serum glucose and lipid profile were observed in the geraniol treated group than negative control group. Weight of organs and adipose tissue isolated from different regions of the body was reduced in geraniol treated group than negative control. Moreover, geraniol interact with HMG-CoA reductase having binding energy -5.13.

Conclusions: In conclusion, data of the report reveals that geraniol reduces obesity by promoting the conversion of white adipose tissue (WAT) to brown adipose tissue (BAT), as it interacts with HMG-CoA reductase in HFD induced obesity in rats.

Aims: Type 1 diabetes (T1D) is an autoimmune disorder that destroys insulin-generating pancreatic β-cells. Preserving pancreatic β-cell function is important for treating T1D. Our study aims to explore the mechanism underlying urolithin C (UC)-mediated regulation of β-cell function.

Methods: Non-obese diabetic (NOD) mice were administrated with UC to evaluate UC-mediated protection of T1D. The inflammation of the pancreas islets was examined by hematoxylin and eosin staining. Glucose-stimulated insulin secretion (GSIS) assay and oral glucose tolerance test were applied to evaluate the progression of T1D. MIN6 cells were treated with TNF-α, IL-1β and IFN-γ in the presence of UC. Cell viability was analyzed by CCK-8. Cell apoptosis, proliferation and DNA fragmentation were examined by Annexin V-FITC and PI staining, EdU incorporation and comet assays. Keap1, Nrf2, HO-1 and NQO1 were examined by western blot. Immunofluorescence staining was applied to detect Nrf2 and insulin.

Results: UC administration significantly reduced diabetes incidence, attenuated insulitis, elevated insulin levels and GSIS and reduced blood glucose and AUC in NOD mice. Cytokine treatment suppressed MIN6 cell viability and proliferation but enhanced apoptosis and DNA damage, and these detrimental effects were relieved by UC treatment. Furthermore, UC administration inhibited Keap1 expression and promoted the expression of Nrf2, HO-1 and NQO1 in NOD mice. Nrf2 signaling has been reported to be implicated in preventing the onset of diabetes, and HO-1 and NQO1 are phase II antioxidant enzymes that are regulated by Nrf2 signaling. Cytokine treatment upregulated Keap1 and downregulated Nrf2, HO-1 and NQO1 in MIN6 cells, but it was reversed by UC. The nuclear translocation of Nrf2 was prevented by cytokine treatment, but UC promoted its nuclear translocation. UC-mediated upregulation of Nrf2, HO-1 and NQO1, decreased cell apoptosis and increased proliferation and insulin secretion were abolished by silencing of Nrf2.

Conclusion: UC improves pancreatic β-cell function by activating Nrf2 signaling, thereby alleviating T1D progression.

Background: Dietary management has been recommended as the cornerstone of type 2 diabetes mellitus (T2DM) management. However, low adherence to dietary recommendations has been identified in both developed and developing countries. Previous research suggests that inhibitory control influences eating behavior, but few studies have been conducted in patients with T2DM. Thus, we aimed to explore the relationship between inhibitory control and dietary adherence among patients with T2DM.

Methods: A total of 393 patients with T2DM from the endocrinology departments of three tertiary hospitals in China were enrolled by the convenience sampling method. Dietary adherence was measured by the Dietary Behavior Adherence Scale for Patients with Type 2 Diabetes Mellitus. Additionally, inhibitory control was subjectively measured by the Behavior Rating Inventory of Executive Function-Adult version (BRIEF-A) and objectively assessed by the stop signal task (SST) and the Stroop task. The relationship between inhibitory control and dietary adherence was analyzed using Pearson correlation analysis and hierarchical regression analysis.

Results: Subjectively measured inhibitory control had a significant predictive effect for dietary adherence after controlling for demographic and clinical variables. Adding the inhibitory control variable to the regression equation resulted in the following values: overall model F (19, 373) = 7.096, p < 0.001, increase in R² value by 0.069, change in F (1, 373) = 35.219, p < 0.001. Similarly, the performance of the Stroop task had a significant predictive effect for dietary adherence to some foods, i.e., carbohydrate and fat. Adding the Stroop effect variable to the regression equation resulted in the following values: overall model F (19, 81) = 2.848, p = 0.005, increase in R² value by 0.060, change in F (1, 81) = 8.137, p = 0.006.

Conclusions: Inhibitory control was a predictor of dietary adherence in patients with T2DM. Future interventions should investigate whether inhibitory control training results in the improvement of dietary adherence in patients with T2DM.

Background: Gestational Diabetes Mellitus (GDM) is hyperglycaemia first detected during pregnancy. Globally, GDM affects around 1 in 6 live births (up to 1 in 4 in low- and middle-income countries- LMICs), thus, urgent measures are needed to prevent this public health threat.

Objective: To determine the effectiveness of pre-pregnancy lifestyle in preventing GDM.

Methods: We searched MEDLINE, Web of science, Embase and Cochrane central register of controlled trials. Randomized control trials (RCTs), case-control studies, and cohort studies that assessed the effect of pre-pregnancy lifestyle (diet and/or physical activity based) in preventing GDM were included. Random effects model was used to calculate odds ratio (OR) with 95% confidence interval. The Cochrane ROB-2 and the Newcastle-Ottawa Scale were used for assessing the risk of bias. The protocol was registered in PROSPERO (ID: CRD42020189574) RESULTS: Database search identified 7935 studies, of which 30 studies with 257,876 pregnancies were included. Meta-analysis of the RCTs (N = 5; n = 2471) in women who received pre-pregnancy lifestyle intervention showed non-significant reduction of the risk of developing GDM (OR 0.76, 95% CI: 0.50-1.17, p = 0.21). Meta-analysis of cohort studies showed that women who were physically active pre-pregnancy (N = 4; n = 23263), those who followed a low carbohydrate/low sugar diet (N = 4; n = 25739) and those women with higher quality diet scores were 29%, 14% and 28% less likely to develop GDM respectively (OR 0.71, 95% CI: 0.57, 0.88, p = 0.002, OR 0.86, 95% CI: 0.68, 1.09, p = 0.22 and OR 0.72, 95% CI 0.60-0.87, p = 0.0006).

Conclusion: This study highlights that some components of pre-pregnancy lifestyle interventions/exposures such as diet/physical activity-based preparation/counseling, intake of vegetables, fruits, low carbohydrate/low sugar diet, higher quality diet scores and high physical activity can reduce the risk of developing gestational diabetes. Evidence from RCTs globally and the number of studies in LMICs are limited, highlighting the need for carefully designed RCTs that combine the different aspects of the lifestyle and are personalized to achieve better clinical and cost effectiveness.

Background and aims: Sarcopenia is associated with worse prognosis for non-alcoholic fatty liver disease (NAFLD). However, disease progression in the MAFLD-related sarcopenia is largely unknown. We aimed to clarify the relationship between MAFLD and/or sarcopenia with mortality and liver fibrosis in the real world.

Methods: A total of 13,692 individuals were selected from the third National Health and Nutrition Examination Surveys and linked mortality until December 2019. MAFLD is diagnosed based on a radiologically diagnosed hepatic steatosis and the presence of any one of the following three conditions: overweight/obesity, diabetes mellitus (DM), or metabolic dysregulation. Sarcopenia is defined by weight-adjusted skeletal muscle mass.

Results: The mean age was 43.7 ± 15.97 years, and 47.3% of the individuals were male. MAFLD was diagnosed in 4207/13,692 (30.73%) participants, and the proportion of sarcopenic was 19.42% amongst subjects with MAFLD. The mean follow-up duration was of 23.7 ± 7.62 years. MAFLD (aHR 1.152, 95% CI 1.070-1.241) and sarcopenia (aHR 1.123, 95% CI 1.042-1.210) were related to increased all-cause mortality in MAFLD after adjustment for age, sex, race, marital status, education, and smoking. Stratified analysis revealed that MAFLD and sarcopenia additively increased the risk of mortality (aHR 1.247, 95% CI 1.132-1.373) and liver fibrosis (aOR 2.296, 95% CI 1.718-3.069 assessed by NFS score >0.676; aOR 2.218, 95% CI 1.788-2.752 assessed by FIB-4 score >1.3) in fully adjusted models (P < 0.001 for all).

Conclusion: Sarcopenia in individuals with MAFLD portends increased mortality and significant liver fibrosis. Novel therapeutic strategies targeting at increasing skeletal muscle mass should be explored for patients with MAFLD.

Background/objectives: Nutrition and obesity researchers often dichotomize or discretize continuous independent variables to conduct an analysis of variance to examine group differences. We describe consequences associated with dichotomizing and discretizing continuous variables using two cross-sectional studies related to nutrition.

Subjects/methods: Study 1 investigated the effects of health literacy and nutrition knowledge on nutrition label accuracy (n = 612). Study 2 investigated the effects of cognitive restraint and BMI on fruit and vegetable (F/V) intake (n = 586). We compare analytic approaches where continuous independent variables were either discretized/dichotomized or analyzed as continuous variables.

Results: In Study 1, dichotomization of health literacy and nutrition knowledge for 2 × 2 ANOVA revealed health literacy had an effect on nutrition label accuracy. Nutrition knowledge has an effect on nutrition label accuracy, but the health literacy by nutrition knowledge interaction was not significant. When analyzed using regression, the nutrition knowledge effect was significant. The simple effect of health literacy was also significant when health literacy equals zero. Finally, the quadratic effect of health literacy was negative and significant. In Study 2, dichotomization and discretization of cognitive restraint and BMI were used for three ANOVAs, which discretized BMI in three ways. For all ANOVAs, the BMI main effect for predicting fruit and vegetable intake was significant, the interaction between BMI and cognitive restraint was non-significant, and cognitive restraint was only significant when both variables were dichotomized. When analyzed using regression, the continuous mean-centered variables, and their interaction each significantly predicted F/V intake.

Conclusions: Dichotomizing continuous independent variables resulted in distortions of effect sizes across studies, an inability to assess the quadratic effect of health literacy, and an inability to detect the moderating effect of BMI. We discourage researchers from dichotomizing and discretizing continuous independent variables and instead use multiple regression to examine relationships between continuous independent and dependent variables.

Background: Fenofibrate is a hypolipidemic peroxisome proliferator-activated receptor α (PPARα) agonist used clinically to reduce hypercholesterolemia and hypertriglyceridemia.

Objective: We investigated the effects of fenofibrate on insulin resistance and tissue inflammation in a high-fat diet (HFD)-fed ovariectomized (OVX) C57BL/6J mice, a mouse model of obese postmenopausal women.

Methods: Female OVX mice were randomly divided into 3 groups and received a low-fat diet, an HFD, or an HFD supplemented with 0.05% (w/w) fenofibrate for 9 weeks. Parameters of insulin resistance and tissue inflammation were measured using blood analysis, histological analysis, immunohistochemistry, and quantitative real-time polymerase chain reaction.

Results: When fenofibrate was administered to HFD-fed OVX mice for 9 weeks, we observed reductions in body weight gain, adipose tissue mass, and the size of visceral adipocytes without the change of food intake. Fenofibrate improved mild hyperglycemia, severe hyperinsulinemia, and glucose tolerance in these mice. It also reduced pancreatic islet size and insulin-positive β-cell area to levels similar to those in OVX mice fed a low-fat diet. Concomitantly, administration of fenofibrate not only suppressed pancreatic lipid accumulation but also decreased CD68-positive macrophages in both the pancreas and visceral adipose tissue. Treatment with fenofibrate reduced tumor necrosis factor α (TNFα) mRNA levels in adipose tissue and lowered serum TNFα levels.

Conclusion: These results suggest that fenofibrate treatment attenuates insulin resistance in part by reducing tissue inflammation and TNFα expression in HFD-fed OVX mice.

Background/objectives: To date, evidence regarding the protective roles of the Mediterranean-Dietary Approaches to Stop Hypertension Intervention for Neurodegenerative Delay (MIND) diet in patients with type 2 diabetes mellitus (T2DM) is scarce. This study aims to estimate the impact of adhering to the MIND diet on the mortality in patients with and without T2DM.

Subjects/methods: In this cohort study, 6887 participants (1021 patients with T2DM) from the NHANES dataset were analyzed. The exposure is the MIND diet adherence. The primary outcomes are all-cause and cardiovascular (CV) deaths.

Results: We documented 1087 all-cause deaths consisting of 377 CV deaths during the follow-up (median time of 10 years). Among participants with T2DM, those with a high MIND score (> 8.0, range of MIND score: 4.5-13) had a significantly lower risk of all-cause death (hazard ratio [HR] 0.75, 95% confidence interval [CI]: 0.59, 0.96, P = 0.021) and CV death (HR 0.50, 95% CI: 0.29, 0.87, P = 0.014) compared to those with a low MIND score (≤ 8.0). In participants without T2DM, a high MIND score was associated with a significant decrease in the risk of all-cause death (HR = 0.83, 95% CI: 0.70, 0.99, P < 0.001), but the association with CV death risk was not statistically significant.

Conclusion: This study uncovered significant associations between the MIND diet and decreased risk of all-cause and CV death in patients with T2DM. The findings highlight the potential benefits of following the MIND diet in managing and enhancing the outcomes of individuals with T2DM.

Background: 5-Aminovaleric acid betaine (5-AVAB) has recently been identified as a diet and microbial-dependent factor inducing obesity and hepatic steatosis in mice fed a Western diet. Accumulating evidence suggests a role in metabolic dysfunction associated with obesity, diabetes, and fatty liver disease. However, whether 5-AVAB plays a role in human disease is unclear, and human data are sparse.

Methods: We measured circulating 5-AVAB serum levels in 143 individuals with overweight or obesity participating in a randomized intervention study (NCT00850629) investigating the long-term effect of a weight maintenance strategy after diet-induced weight reduction.

Results: Higher 5-AVAB serum levels correlate with worse estimates of obesity, glucose metabolism, and hepatic steatosis after weight loss. Furthermore, higher 5-AVAB levels after weight loss independently predict detrimental changes in glucose metabolism 18 months after the successful weight reduction.

Conclusion: Our human data supports previous findings in rodents indicating a relevant, potentially disadvantageous function of 5-AVAB in the context of metabolic dysbalance.

Background/objectives: Despite the evidence supporting the efficacy of the ketogenic diet (KD) on weight and type 2 diabetes (T2D) management, adherence to the KD is challenging. Additionally, no studies have reported changes in PA among individuals with overweight/obesity and T2D who have followed KD. We mapped out the methods used to assess adherence to the KD and level of physical activity (PA) in lifestyle interventions for weight and T2D management in individuals with overweight/obesity and T2D and compared levels of KD adherence and PA in these interventions.

Methods: Articles published between January 2005 and March 2022 were searched in MEDLINE, CINAHL, and Scopus. Studies that included KD in lifestyle interventions for adults with T2D and overweight/obesity and measured ketone levels were included.

Results: The eleven included studies comprised eight randomized controlled trials. They mainly used self-reported measures to evaluate adherence to the KD and level of PA. We found studies reported higher carbohydrate intake and lower fat intake than the KD regimen. Great inconsistencies were found among studies on the measurement and reporting of ketone and PA levels.

Conclusion: Our results demonstrated the need to develop intervention strategies to improve adherence to the KD, as well as the necessity of developing standardized diet and PA assessment tools to establish a stronger evidence base for including KD in lifestyle interventions for weight and T2D management among adults with overweight/obesity and T2D.