Women with type 2 diabetes mellitus (T2DM) often require interventions that are culturally acceptable, practical, sustainable, and can be easily fit into their daily routine to manage their blood sugar levels. Although plant-based dietary patterns and time-restricted fasting have demonstrated metabolic benefits, limited evidence exists on their combined effects in Indian women with T2DM. This trial evaluated whether a lactovegetarian diet combined with 14-hour time-restricted eating improves glycemic and cardiometabolic outcomes compared with usual diabetes care. 96 women (25–60 years) with T2DM were enrolled in a 24-week, multicenter, randomized, open-label parallel-arm trial; 90 completed the study. The participants were divided into two groups: an intervention group following a structured lacto-vegetarian diet combined with 14-hour fasting, and control group receiving usual diabetes care. The diet contained 15–20% protein, 20–25% fat, and improved carbohydrate quality (50–55% from whole grains/high-fiber foods). Biochemical estimations and anthropometric measurements were taken at baseline and 24 weeks. The study employed an intention-to-treat analysis protocol, and the perceived benefits and safety of the intervention were reported. At 24 weeks, baseline-adjusted between-group comparisons showed significantly greater improvements in the intervention group compared with usual diabetes care. The intervention group had lower adjusted values for body weight, BMI, glycemic, and lipid profiles. The adjusted mean HbA1c was 6.53% in the intervention group compared with 7.65% in the control group, with an adjusted mean difference of −1.12% (95% CI: −1.35 to −0.89; p < 0.001). HOMA-IR was also significantly lower in the intervention group, with an adjusted mean difference of −1.84 (95% CI: −2.27 to −1.41; p < 0.001). Adverse events were mild and transient, while most participants reported improved energy, mood, weight loss, and overall health. A culturally adaptable lacto-vegetarian diet combined with a 14-hour time-restricted fasting regimen safely improves metabolic control and insulin sensitivity in women with Type 2 Diabetes, offering a practical, women-centric strategy that may be implementable within structured clinical nutrition services, although its staffing requirements, cost, and scalability require further evaluation. CTRI/2024/09/073262, Ethical Approval by Institutional Committee: SIU/IEC/781A
Mesenchymal stem cells (MSCs) have demonstrated therapeutic potential in diabetic nephropathy (DN), yet the underlying mechanisms remain incompletely understood, limiting strategies to enhance their efficacy. This study aimed to elucidate whether MSCs exert renoprotective effects by modulating the gut microbiota and its metabolite short-chain fatty acids (SCFAs). DN was induced in rats via a high-fat diet (HFD) combined with streptozotocin (STZ) injection. MSCs were administered via tail vein infusion. Therapeutic efficacy was evaluated by renal function parameters, urine biochemistry, and renal histopathology. Neutrophil extracellular trap (NET) formation was assessed using immunofluorescence staining and ELISA. Alterations in gut microbial composition and SCFA profiles were analyzed through 16S rRNA gene sequencing and targeted metabolomics, respectively. The causal role of the gut microbiota was validated using fecal microbiota transplantation (FMT). Administration of MSCs, as well as FMT from MSC-treated donors, significantly ameliorated renal injury and suppressed NET formation in DN rats. Notably, pharmacological induction of NETs abolished the protective effects conferred by MSC-FMT. 16S rRNA sequencing revealed that MSC intervention enriched beneficial bacterial populations, particularly within the family Muribaculaceae. Targeted metabolomic analysis identified a significant elevation of butyrate among fecal SCFAs in MSC-treated rats. Furthermore, exogenous butyrate supplementation recapitulated the inhibitory effects on NET formation and attenuated DN progression. MSC therapy alleviates diabetic nephropathy via a gut-kidney axis mechanism, driven by the enrichment of butyrate-producing microbiota and the subsequent inhibition of neutrophil extracellular trap formation.
Type 2 diabetes mellitus (T2DM) is marked by hyperglycemia, oxidative stress, and systemic inflammation. Prebiotics, such as bitter almond gum (Amygdalus communis L. var. amara), have the potential to influence gut microbiota and metabolic parameters, suggesting their role as dietary interventions for enhancing glycemic control in the management of T2DM. This study evaluated the effects of bitter almond gum on glycemic indices, oxidative stress, and oxidant biomarkers in individuals with T2DM. This randomized, triple-blinded, placebo-controlled, clinical trial included 44 women with T2DM. They were assigned to either the intervention (n = 22) or control (n = 22) groups receiving 5 g per day of bitter almond gum or maltodextrin, respectively, for a duration of 8 weeks. Various outcomes, including glycemic indices, lipopolysaccharide (LPS) levels, oxidative stress markers, and antioxidant biomarkers, were measured at baseline and again after 8 weeks. Bitter almond gum supplementation significantly reduced insulin levels (−1.23 mg/dL; 95% CI, [–2.40, –0.03]), LPS ( − 6.32 mg/dL; 95% CI, [–9.51, –3.09]), pentosidine (−38.02 mg/dL; 95% CI, [–55.18, –20.71]), and oxidative stress index (OSI) (−5.59 mg/dL; 95% CI, [–10.81, –0.30]), and increased McAuley_index (0.20 mg/dL; 95% CI, [0.14, 0.32]), total antioxidant capacity (TAC) (0.18 mg/dL; 95% CI, [0.07, 0.26]), superoxide dismutase (SOD) (180.20 mg/dL; 95% CI, [65.27, 295.14]), and glutathione peroxidase (GSH-Px) (2.21 mg/dL; 95% CI, [0.78, 3.62]) compared with the placebo group (P < 0.05, ANCOVA adjusted for baseline and confounding factors). Bitter almond gum supplementation for 8 weeks led to improvements in glycemic control, a reduction in oxidative stress, and an enhancement of antioxidant defenses in women with T2DM. These findings indicate its potential as a complementary functional food for managing diabetes.
Diets high in fat, specifically saturated fatty acids, can reduce muscle capillary density and blunt insulin-induced muscle microvascular blood flow (MBF), limiting nutrient delivery to the myocytes, increasing metabolic and vascular disease risk. However, effects of polyunsaturated fatty acids (PUFA) on these outcomes remain unclear. This systematic review aimed to summarize current evidence on the effects of PUFA on muscle capillary density and MBF. A systematic search of Medline Complete, PubMed, Embase, and the Cochrane Library identified studies examining PUFA interventions and microvascular outcomes. The outcomes included capillary density, capillary-to-fiber ratio, and peripheral, arteriolar, or microvascular perfusion in skeletal muscle. Of 1705 records screened, 12 studies met the inclusion criteria (9 animal and 3 human studies). In animal models, n-3 PUFA supplementation, primarily as fish oil, improved muscle capillary density and prevented impairments in MBF induced by ischemia or endotoxin infusion. These effects were potentially mediated through increased vascular endothelial growth factor, nitric oxide, and prostacyclin production. In contrast, n-6 PUFA showed no consistent benefits. Human studies in this area are very limited. Overall, animal studies suggest n-3 PUFA may enhance skeletal muscle microvascular function, but well-designed human studies are needed to confirm these findings.
Carotenoids, a class of antioxidant phytochemicals, have been proposed to influence adiposity and metabolic regulation through modulation of oxidative stress, inflammation, and adipokine secretion. However, clinical evidence remains inconsistent. This systematic review and meta-analysis aimed to quantitatively evaluate the effects of carotenoid supplementation on anthropometric and adipokine parameters, including body weight, body mass index (BMI), waist circumference (WC), hip circumference (HC), body fat percentage, fat-free mass (FFM), leptin, and adiponectin. Following PRISMA 2020 guidelines, randomized controlled trials (RCTs) published up to October 2025 were identified through PubMed, Scopus, Embase, and Web of Science. Weighted mean differences (WMDs) with 95% confidence intervals (CIs) were calculated using random-effects models. Heterogeneity and publication bias were assessed via I² statistics and Egger’s test, respectively. Twenty-seven RCTs were included. Carotenoid supplementation significantly reduced body weight (WMD: –1.00 kg; 95% CI: –1.87 to –0.13) and WC (–1.78 cm; 95% CI: –3.02 to –0.54), while increasing FFM (+2.32 kg; 95% CI: +0.49 to +4.14). Furthermore, leptin levels decreased significantly (–1.42 ng/mL; 95% CI: –2.35 to –0.49), whereas BMI, adiponectin, HC, and total body fat percentage showed no significant changes. Subgroup analyses revealed stronger effects in interventions lasting >8 weeks and in participants aged <50 years. No substantial publication bias was detected. Carotenoid supplementation exerts modest but favorable effects on body composition and leptin regulation, supporting its potential as an adjunct in metabolic health improvement. Longer, high-quality RCTs are warranted to confirm these findings and clarify dose–response relationships.
eHealth lifestyle interventions have emerged as promising management strategies for metabolic dysfunction-associated steatotic liver disease (MASLD). Our review aimed to synthesize the most recent evidence to evaluate the effectiveness of eHealth lifestyle interventions on clinical and behavioral outcomes in adults with MASLD. Twelve databases (Medline, Web of Science Core Collection, Embase, Cochrane Central Register of Controlled Trials, ProQuest Health & Medical Collection, CINAHL Complete, Academic Search Complete, Scopus, Emerald, China National Knowledge Infrastructure, Wanfang Data, and VIP Database) were searched from inception to April 2, 2025. Thirteen randomized controlled trials and fifteen quasi-experimental trials comprising 2579 adult patients with MASLD were included. Seven intervention components were identified: goal setting, health education, consultation, self- and device-monitoring, feedback, patient reminders, and social support. Meta-analysis of randomized controlled trials demonstrated that eHealth lifestyle interventions were significantly superior to standard care in reducing weight, body mass index, waist circumference, alanine aminotransferase, aspartate aminotransferase, and γ-glutamyl transferase levels, and improving MASLD status. Improvements in self-management, dietary adherence, physical activity, exercise, and quality of life were also observed. Our findings suggest that ehealth intervention is a better choice for the patients with MASLD to achieve precise and scalable management. PROSPERO CRD420251001470. PROSPERO CRD420251001470; https://www.crd.york.ac.uk/PROSPERO/view/CRD420251001470.
To investigate the association between an almond-based low-carbohydrate diet (LCD) and continuous glucose monitoring (CGM) metrics in patients with type 2 diabetes mellitus (T2DM). This was a prospective randomized controlled study. Hospitalized patients with T2DM from Changshu No.1 People’s Hospital were recruited from January 2022 to December 2022. 33 patients using CGM were included and randomly divided into the low-fat diet (LFD) group or the LCD with almonds group based on the random number table. Primary CGM metrics including time in range (TIR), time in tight range (TITR), time above range (TAR), time below range (TBR) were compared between the two groups. Linear regression analysis was performed to assess the association between diet group and nocturnal glycemic metrics. Compared to LFD group, patients in the LCD with almonds group had higher nighttime TIR [98.51% (95.83, 99.88) vs. 91.67% (89.52, 98.07), P < 0.01] and TITR [94.14% (87.57, 98.41) vs. 77.58% (52.18, 90.58), P < 0.05]. Nighttime TAR [0.00% (0.00, 0.00) vs. 1.39% (0.00, 7.95), P < 0.01], HBGI [0.15 (0.01, 0.34) vs. 0.98 (0.08, 3.73), P < 0.05], and SD (15.57 ± 6.21 mg/dL vs. 23.62 ± 9.12 mg/dL, P < 0.05) were significantly lower in the LCD with almonds group. Multivariable regression demonstrated that LCD with almonds was independently associated with improvements in nocturnal TIR (β = 6.65%, P = 0.010) and TITR (β = 14.60%, P = 0.016) after adjustment for age, sex, and diabetes duration. The almond-based low-carbohydrate diet improved nocturnal glycemic control in patients with type 2 diabetes. These improvements in nocturnal TIR and TITR remained significant after multivariable adjustment for age, sex, and diabetes duration. The study was registered at clinicaltrials.gov (registration no. ChiCTR2600116495).
OBJECTIVES:Existing evidence links diet and the oral microbiota to individual cardiovascular, kidney, and metabolic conditions, but these relationships have not been extended to the progressive stages of cardiovascular-kidney-metabolic (CKM) syndrome. We therefore investigated the associations among dietary patterns, the oral microbiome, and CKM stages. METHODS:This cross-sectional study included 2051 representative US adults. Oral microbiota was characterized via 16S rRNA gene sequencing of oral rinse samples. Dietary patterns were assessed using multiple dietary indexes derived from 24-h dietary recalls. CKM stages were defined according to American Heart Association criteria. MaAsLin3 analysis and ordinal logistic regression were used to evaluate the associations of dietary indexes and oral microbiota with CKM stages. Mediation analysis was used to assess the mediating role of oral microbiota in the associations between various dietary indexes and CKM stages. RESULTS:As CKM stages advanced, the oral microbial community tended to exhibit gradient shifts, primarily characterized by a potentially progressive reduction in the relative abundance of Pseudomonadota. Neisseria and Lautropia within Pseudomonadota, together with Gemella and Bergeyella, were negatively associated with CKM stages, whereas Lactobacillus was positively associated. Pseudomonadota-dominated salivatypes were associated with the lowest risk of advanced CKM stages. Higher healthy dietary indexes were associated with lower likelihood of advanced CKM stages and with higher abundance of Pseudomonadota taxa, particularly Neisseria. Notably, Neisseria and its higher taxonomies predominantly mediated the associations between dietary indexes and CKM stages. CONCLUSION:This study suggests that Neisseria-related taxa are predominant mediators linking dietary patterns to CKM stages. Modulation of the diet-microbiome axis may represent a complementary strategy for promoting health and potentially influencing CKM-associated outcomes, but our cross-sectional data should not be interpreted as establishing a causal protective role.
BACKGROUND:The ketogenic diet (KD) is a widely used nutritional intervention for weight loss. The beneficial effects of the KD are intrinsically linked to the state of physiological ketosis, where ketone bodies (KBs) raise, even though minimal effective threshold of blood ketone concentration that correlates with significant weight loss remains unclear. Therefore, the main purpose of this study was to identify the optimal β-hydroxybutyrate (βHB) threshold associated with weight loss in individuals with overweight or obesity undergoing a KD. METHODS:This secondary analysis included 217 participants (111 males and 106 females) with overweight or obesity, who followed a KD for 14 days. Time to Ketosis (TtK)-defined as the number of days needed to reach and maintain a given ketone concentration-was calculated for each threshold. RESULTS:Regression analysis showed that a βHB concentration of ≥0.5 mmol/L was the most associated with significant weight loss. Moreover, body weight and gender significantly influenced TtK, suggesting interindividual variability in achieving effective ketosis. CONCLUSIONS:Achieving and maintaining a ketonemia of at least 0.5 mmol/L may represent a clinically meaningful threshold to optimize weight loss in individuals undergoing a KD. Monitoring βHB levels and reducing TtK may improve individual responsiveness to KD-based interventions.
BACKGROUND/OBJECTIVES:Colorectal cancer (CRC) is influenced by genetic, environmental, and dietary factors, with increasing evidence highlighting the role of the gut microbiota in its development. Probiotics, prebiotics, and fermented foods such as yogurt have been recognized for their ability to promote gut microbial balance and potentially reduce CRC risk. This study try to investigate the association between the consumption of these dietary components and CRC prevalence among adults aged 50 years and older. SUBJECTS/METHODS:This study analyzed data from the National Health and Nutrition Examination Survey (NHANES) from 2001 to 2020. Dietary intake was assessed using the Food Frequency Questionnaire and the 30-Day Dietary Supplement Use Questionnaire, while CRC history was based on self-reported diagnoses. Multivariable logistic regressions were applied, adjusting for demographic characteristics (age, sex, race/ethnicity, poverty income ratio, education), lifestyle factors (smoking status, total energy intake, red meat intake, total dietary fiber intake), and clinical variables (BMI, cardiovascular disease, chronic kidney disease, fasting plasma glucose, and serum albumin). RESULTS:The final analytic sample included 9405 participants, representing an estimated 37 million U.S. adults. After adjustment, consumption of probiotics, prebiotics, or yogurt was associated with approximately 50% lower odds of CRC (adjusted odds ratio = 0.50; 95% CI: 0.29-0.88). CONCLUSIONS:These findings indicate a potential protective association of these dietary components with CRC, likely mediated through modulation of the gut microbiota. While the cross-sectional design limits causal interpretation, the results support existing literature on the beneficial role of diet in cancer prevention. Further longitudinal studies are necessary to confirm these associations and inform public health strategies aimed at reducing CRC risk through targeted dietary interventions.
BACKGROUND:Identifying differentially expressed miRNAs in plasma-derived exosomes associated with type 2 diabetes mellitus (T2DM) complicated by atherosclerosis (AS) and elucidating their roles in high-glucose/high-lipid-induced vascular endothelial dysfunction. METHODS:Plasma-derived exosomal miRNAs were isolated from people with T2DM complicated by AS and healthy controls. Followed by miRNA sequencing to characterize differential expression profiles between groups. GO and KEGG pathway enrichment analyses were performed on differentially expressed miRNAs. Human umbilical vein endothelial cells (HUVECs) were exposed to combined hyperglycemia and hyperlipidemia to establish an in vitro model of diabetic endothelial injury. HUVECs were subsequently transfected with miR-887-5p mimics, inhibitors or negative controls, and assessed for proliferation, migration, apoptosis, oxidative stress, and nitric oxide (NO) content. RESULTS:Sequencing revealed globally reduced plasma exosomal miRNA expression in people with T2DM and AS relative to healthy controls, with 21 upregulated and 23 downregulated miRNAs identified. Among these, hsa-miR-887-5p exhibited the greatest fold change of all detected miRNAs, while hsa-miR-96-5p and hsa-miR-183-5p (upregulated) and hsa-miR-410-3p (downregulated) harbored the most target genes implicated in diabetic atherosclerosis. Functionally, miR-887-5p enhanced HUVEC proliferation and migration under high-glucose/high-lipid conditions, elevated superoxide dismutase (SOD) activity, reduced lactate dehydrogenase (LDH) and malondialdehyde (MDA) levels, suppressed intracellular iNOS/NO and attenuated apoptosis. CONCLUSION:Plasma exosomal miRNA expression is broadly reduced in people with T2DM complicated by AS. hsa-miR-887-5p, hsa-miR-96-5p, hsa-miR-183-5p, and hsa-miR-410-3p may emerge as candidates with diagnostic and therapeutic relevance in this context. Specifically, miR-887-5p mitigates high-glucose/high-lipid-induced vascular endothelial injury, warranting further investigation as a therapeutic target.
OBJECTIVE:To evaluate the heterogeneity of treatment effects (HTEs) of intensive lifestyle intervention (ILI) in adults with type 2 diabetes and overweight/obesity, and identify a subgroup with greater cardiovascular benefits from ILI. METHODS:In a post-hoc analysis of the Look AHEAD trial, causal forest modeling was used to identify HTEs of ILI. The study population was stratified into four subgroups, and the associations of ILI with cardiovascular outcomes were assessed using multivariable Cox modeling compared to diabetes support & education (DSE). RESULTS:Among 4710 participants (mean age 58.9 years, 58.5% women), 768 primary outcomes occurred over a median follow-up of 9.5 years. Key variables identified through causal forest modeling were SF-36 mental health, diabetes duration, and urine albumin-creatinine ratio (ACR). In Subgroup 4 (SF-36 mental health > 55.64 and ACR > 10 mg/g), which had more cardiovascular risk factors and comorbidities, ILI significantly reduced the primary outcome risk (HR: 0.65, 95% CI: 0.48-0.87, P = 0.004) and three secondary outcomes compared to DSE. No cardiovascular benefits were observed in participants with SF-36 mental health ≤ 55.64 or ACR < 10 mg/g. CONCLUSION:This post-hoc analysis of the Look AHEAD trial showed HTEs of ILI in adults with type 2 diabetes and overweight/obesity. Participants with better mental health, poorer renal function, and more cardiovascular risk factors were more likely to benefit from ILI.
BACKGROUND:Folate (vitamin B9) is a water-soluble vitamin necessary for one-carbon metabolism, supporting the synthesis, repair, and methylation of DNA. While maternal folate status is well-studied for its role in fetal development and metabolic programming, the impact of inadequate folate intake in males on offspring development and metabolic diseases remains poorly understood. This study investigates the effects of folate deficiency in male parents on developing hepatic insulin resistance in offspring, focusing on molecular and metabolic disruptions within the liver. METHODS:Three-week-old C57BL/6 male mice were categorized into two groups: Group I received a folate-normal (FN) diet, and Group II was fed a folate-deficient (FD) diet for four weeks before mating. F1 offspring from Group I (FN diet) were mated to produce F2 offspring (PNMN: paternal normal, maternal normal). F1 males from Group II (lifetime FD diet) were mated with F1 females on an FN diet to produce F2 offspring (PDMN: paternal deficient, maternal normal). F2 offspring from both groups were maintained on an FN diet and monitored for body weight. The study assessed systemic markers of insulin resistance, lipid and glucose metabolism, and gene expression profiles and proteins associated with insulin signaling in the liver. Mechanistic pathways involving lipid-induced and ER stress-triggered hepatic insulin resistance were explored. RESULTS:Male offspring born to folate-deficient fathers (PDMN) exhibited significantly elevated fasting glucose and insulin levels, impaired glucose tolerance, increased HOMA-IR and reduced QUICKI at 10 weeks. Hepatic insulin signaling was disrupted, as evidenced by downregulated p-AKT levels in 7-week PDMN males. Lipogenic pathways were upregulated, with increased expression of transcription factors Srebf1c and Chrebp (both at gene and protein levels), contributing to hepatic steatosis. Gluconeogenic genes, including Foxo1 and Fbp1, were also upregulated, indicating elevated hepatic glucose output and exacerbation of hyperglycemia. Chronic endoplasmic reticulum (ER) stress, marked by upregulation of Perk and Atf6 (both at gene and protein levels), further impaired hepatic insulin signaling possibly by activating stress pathways and disrupting protein folding. CONCLUSION:This study provides the first evidence that paternal folate deficiency predisposes offspring to hepatic insulin resistance by disrupting insulin signaling, promoting lipid dysregulation, and activating ER stress pathways. These effects are more severe in males, underscoring sex-specific susceptibility. The findings emphasize the importance of balanced paternal folate intake during reproduction to prevent intergenerational metabolic disorders and suggest potential therapeutic targets to mitigate hepatic insulin resistance caused by paternal nutritional deficiencies.
BACKGROUND:Evidence from randomised controlled trials shows that vitamin C (VC) supplementation may improve cardiometabolic health outcomes in people with type 2 diabetes (T2D). Plasma proteomics may help to further enhance our understanding of VC's therapeutic effects and biological mechanisms in T2D. Therefore, our aim was to explore the effects of VC supplementation on the plasma proteome in people with T2D. METHODS:A double-blind, placebo-controlled, crossover trial was undertaken in people with T2D, who were administered 1000 mg/day VC or placebo for 4 months. Plasma proteins in 26 participants (22 male, 4 female, age 62.6 ± 6.5 years, HbA1c 60 ± 11 mmol/mol [7.6 ± 0.7%]) were quantified by liquid chromatography/mass spectrometry with data-independent acquisition. Differential protein expression was assessed for VC post-supplementation vs. control [pooling of all non-active conditions]. RESULTS:Twelve proteins were significantly downregulated and three were upregulated following VC supplementation (|log2-fold change [FC]| ≥ 0.5; false discovery rate<0.05). These included proteins with functions in innate immunity, carbohydrate digestion, unfolded protein binding, and muscle contraction. Protein candidates that had the greatest magnitude decrease (|log2-FC| > 1) with VC supplementation were alpha-amylase 1 (AMY1), heat shock protein 75 kDa (TRAP1), myosin-1 (MYH1), and serum amyloid protein A1 (SAA1). Pathway enrichment revealed underrepresentation of unfolded protein binding, ATP binding, attenuation phase, and the innate immune system following VC supplementation. TRAP1, alpha-actin-1, Heat shock 70 kDa protein-1, and CD166 antigen were associated with previously reported improved blood-pressure outcomes following VC supplementation. CONCLUSIONS:VC supplementation significantly altered abundance of numerous proteins in plasma, with functions relating to the innate immune system, dietary carbohydrate digestion, and protein folding chaperone activity. We identified novel proteins responsive to VC supplementation and protein-clinical improvement correlations in people with T2D that require further exploration to understand their biological significance.
Cardiovascular disease (CVD) is a leading cause of morbidity and mortality in patients with type 2 diabetes mellitus (T2DM). Okra (Abelmoschus esculentus), a traditional plant rich in fiber, flavonoids, and antioxidants, has been suggested to improve glycemic control, lipid metabolism, and inflammation, but clinical evidence remains inconsistent. The major objective of our review was to elucidate the impact of okra supplementation on blood pressure, lipid profile, and inflammation in patients with prediabetes, T2DM, and diabetic nephropathy. Eligible studies were identified through PubMed, Embase, Web of Science, and Scopus up to February 17, 2026. Pooled weighted mean differences (WMD) with 95% confidence intervals (CI) were calculated using random-effects models. Ten studies were included. Okra supplementation significantly reduced total cholesterol (14.16 mg/dL, 95% CI: -22.39, -5.92, P < 0.001), LDL-C (-8.51 mg/dL, 95% CI: -14.92, -2.11, P = 0.009), triglycerides (-15.43 mg/dL, 95% CI: -28.67, -2.19, P = 0.022), diastolic blood pressure (-1.17 mmHg; 95% CI: -2.28 to -0.06), and CRP (-2.28 mg/dL; 95% CI: -2.70 to -1.86). No significant effects were observed for systolic blood pressure or HDL-C overall. Okra supplementation exerts beneficial effects on lipid profiles, diastolic blood pressure, and systemic inflammation in individuals with prediabetes, T2DM, and diabetic nephropathy, suggesting a potential role as an adjunctive therapy for reducing CVD risk.
BACKGROUND:This trial evaluated the combined effect of yoga and camelina sativa powder (CSP) on glycemic indices, inflammatory and oxidative stress parameters in women with type 2 diabetes mellitus (T2DM). METHODS:In this trial, 80 patients with T2DM were randomly allocated into four groups: group 1 (placebo), group 2 (receiving CSP), group 3 (doing yoga), and group 4 (receiving CSP and doing yoga) for 8 weeks. Glycemic indices, inflammatory and oxidative stress parameters were assessed pre-and post-intervention. RESULTS:CSP plus yoga treatment significantly increased the McAuley-index and Quick-index compared to the placebo group (P = 0.021 and P < 0.001, respectively). A significant decrease in the glycemic exposure (GE) index (P = 0.010), fasting blood sugar (FBS) (P = 0.003), hemoglobin A1c (P = 0.013), insulin (P = 0.002), and homeostasis model assessment of insulin resistance (HOMA-IR) (P < 0.001) was found in the CSP plus yoga group compared to the placebo after adjustment for confounders. Serum superoxide dismutase level significantly increased in camelina, yoga, and both CSP plus yoga groups compared to the placebo group (P < 0.001, P = 0.019, and P = 0.005, respectively). Serum catalase levels increased significantly in CSP plus yoga group compared to the placebo following 8 weeks (P = 0.022). Malondialdehyde concentration declined significantly in yoga and CSP plus yoga groups compared to placebo (P = 0.017 and P < 0.001, respectively). Serum tumor necrosis factor-α (TNF-α) level significantly decreased in CSP, yoga, and combined CSP plus yoga groups compared with the placebo group (P < 0.001, P = 0.033, and P < 0.001, respectively). CONCLUSION:We found a favorable effect of co-treatment of CSP and yoga for 8 weeks in women with T2DM on some glycemic indices, oxidative stress, and inflammatory parameters. The combined effect of yoga and camelina sativa powder on glycemic indices, inflammation, and oxidative stress. PPAR-γ: peroxisome proliferator-activated receptor gamma, NF-kB: nuclear factor kappa B, GLP: glucagon-like peptide, PYY: peptide YY, SCFA: short chain fatty acids, ROS: reactive oxygen species, LPS: lipopolysaccharides, HPA: hypothalamic-pituitary-adrenal axis.
BACKGROUND/OBJECTIVES:Targeting postprandial glucose response (PPGR) is more effective than lowering fasting plasma glucose in improving glycemic control and reducing cardiovascular risk in individuals with type 2 diabetes (T2D). Continuous glucose monitoring (CGM) has the potential to uncover time-related features of PPGR. This study evaluates the within-subject reproducibility of dynamic PPGR parameters obtained by CGM and explores their potential as independent predictors of glycemic control in T2D. SUBJECTS/METHODS:A total of 102 individuals with T2D underwent a 7-day CGM and consumed a standardized breakfast twice to assess the 4-h glucose response, described by the following parameters: glucose peak-the highest glucose value; time to peak-time of peak occurrence; delta glucose max-the difference between the peak and fasting glucose; nadir-the lowest post-peak glucose value; incremental area under the glucose curve; mean postprandial glucose-the average interstitial glucose concentration. Intraclass correlation coefficients (ICCs) for both single and average measurements with their 95% confidence intervals (CIs), were calculated for PPGR parameters to estimate their within-subject reproducibility. Multivariable linear regression models assessed the independent predictive contribution of PPGR parameters, fasting glucose, and 2-h postprandial glucose on 7-day CGM metrics and HbA1c. RESULTS:Moderate to good reproducibility for single measurements was observed for mean glucose (ICC: 0.78, 95%CI 0.69-0.84), glucose peak (ICC: 0.69, 95% CI 0.57-0.78), and nadir (0.74, 95% CI 0.64-0.82). Mean postprandial glucose was the strongest predictor of 7-day time in range (β = -0.772, p < 0.001), 7-day mean glucose (β = 0.800, p < 0.001) and HbA1c (β = 0.434, p < 0.001), whereas the glucose peak was the main predictor of short-term glycemic variability, as reflected by the 7-day coefficient of variation (β = 0.258, p = 0.006) and mean amplitude of glucose excursions (β = 0.613, p < 0.001). CONCLUSION:In individuals with T2D, CGM-derived parameters of PPGR are reproducible and could represent a practical tool to uncover meaningful information about glucose control, which 2-h postprandial glucose fails to predict.
BACKGROUND:Effective management of fibroblast inflammation and apoptosis caused by high glucose is pivotal for mitigating diabetic foot ulcers (DFUs). Recent studies have indicated the potential involvement of Fibrillin-1 (FBN1) in DFU healing through its impact on fibroblast proliferation, migration, and apoptosis. However, detailed cellular mechanism remained uncleared. METHODS:Three primary fibroblast cultures were established conventionally. The impact of FBN1 was studied through knockdown and overexpression. FBN1 levels were gauged via reverse transcription-quantitative polymerase chain reaction (RT-qPCR for mRNA) and Western blot (for protein). Immunofluorescence localized FBN1. Proliferation was assessed via MTT assays, and EDU staining tracked cell viability. TUNEL detected apoptosis. Inflammation was measured by ELISA. Electron microscopy visualized cellular structure changes linked to autophagy, corroborated by Western blot markers. RESULTS:Fibroblasts exposed to high glucose exhibited dysregulated FBN1 expression and disrupted autophagy. FBN1 overexpression promoted proliferation and suppressed inflammation and apoptosis under high glucose conditions. Additionally, FBN1 was found to restore autophagy inhibited by high glucose. In contrast, FBN1 silencing further suppressed autophagy, thereby aggravating inflammation and apoptosis. CONCLUSION:Dysregulation of FBN1 in fibroblasts induced by high glucose hampers autophagy, ultimately leading to apoptosis and inflammation. The upregulation of FBN1 counters these processes, potentially enhancing the healing of DFUs.
BACKGROUND:To investigate the impact of 1-hour plasma glucose (1 h-PG) on the metabolic characteristics and pregnancy outcomes in polycystic ovary syndrome (PCOS). METHODS:This multicenter study analyzed 970 PCOS patients (2019-2025), including 289 undergoing assisted reproductive technology (198 successful deliveries). Participants were stratified by glucose tolerance: Group 1 (normal: fasting PG [FPG] ≤ 6.1, 1 h-PG < 8.6, 2-hour PG [2 h-PG] <7.8 mmol/L); Group 2 (isolated 1 h-prediabetes: 8.6 ≤ 1 h-PG < 11.6, FPG ≤ 6.1, 2 h-PG < 7.8 mmol/L); Group 3 (traditional 2 h-prediabetes: 7.8 ≤ 2 h-PG ≤ 11.1, FPG ≤ 6.1 mmol/L). Data included anthropometrics, metabolic biomarkers, sex hormones, and pregnancy outcomes were compared across three groups. RESULTS:PCOS with isolated 1 h-prediabetes (Group 2) had a more unfavorable metabolic profile with regard to metabolic traits, but were not significantly different from those of the traditional 2 h-prediabetes (Group 3). The adjusted odds ratios (ORs) for hypertension, hyperlipidemia, metabolic syndrome (MetS), and hyperuricemia in PCOS with Group 2 were 1.451 (1.013-2.079, P = 0.042), 1.706 (1.188-2.450, P = 0.004), 2.957 (1.755-4.981, P < 0.001), 1.890 (1.327-2.692, P < 0.001), respectively. For pregnancy outcomes, PCOS in Group 2 were more likely to progress to gestational diabetes mellitus (GDM) than those of Group 1, which was similarly observed in Group 3. The adjusted OR for GDM in the Group 2 was 4.065 (1.530-10.800, P = 0.005). CONCLUSIONS:Our study demonstrated that similar to 2 h-PG, elevated 1 h-PG was associated with different metabolic disorders and GDM. Therefore, 1 h-PG may serve as an additional marker of adverse metabolic status in women with PCOS.
Obesity presents significant health risks, including metabolic disorders and depressive symptoms, necessitating effective interventions such as sleeve gastrectomy (SG), which enables substantial weight loss and metabolic improvements. The primary question of this study was whether SG also affects faecal short-chain fatty acid (SCFA) profiles over 12 months, and whether these changes are related to anthropometric, biochemical, and psychological parameters. A total of 37 female patients with obesity were included in this prospective, observational study. Patients underwent SG and were followed for 12 months postoperatively. SCFA profiles were analysed by gas chromatography-mass spectrometry (GC-MS). Faecal samples for SCFA analysis, anthropometric measurements, blood biochemical markers, food intake and psychological assessments were collected at baseline and at regular intervals after surgery. Our results indicate that SG leads to significant reductions in body mass index, lipid profiles, and systemic inflammation markers, with concurrent alterations in SCFA concentrations, particularly a decrease in major SCFAs (acetic, propionic, and butyric acids) over time. An increase in branched SCFAs was observed post-surgery, which may reflect shifts in the gut microbiota composition and fermentation processes. Patients also reported improvements in emotional well-being and dietary habits. These findings support the hypothesis that SG induces changes in gut microbiota metabolism and underscore the complex interplay between bariatric surgery, gut microbiota, SCFA metabolism, and psychological health. They highlight the need for further research to clarify the long-term implications of these changes and the mechanisms involved.
