Visceral Fat and Diabetes: Associations With Liver Fibrosis in Metabolic Dysfunction-Associated Steatotic Liver Disease.

Background: The prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD), previously known as non-alcoholic fatty liver disease, is increasing globally. Noninvasive methods, such as bioelectrical impedance analysis (BIA), which measures body composition, including visceral fat, are gaining interest in evaluating MASLD patients. Our study aimed to identify factors associated with significant liver fibrosis, compare noninvasive scores, and highlight the importance of visceral fat measurement using BIA. Methods: MASLD patients seen in our out-patient department underwent comprehensive evaluations, including liver stiffness using transient elastography, body composition analysis using BIA, and metabolic measurements. Significant fibrosis was defined as a liver stiffness measurement of ≥8.2 kPa. Using multivariate analysis, we identified factors associated with significant liver fibrosis and compared four noninvasive scores with a novel diabetes-visceral fat 15 (DVF15) score. Results: We analyzed data from 609 MASLD patients seen between February 2022 and March 2023. The median age was 43 years (81% male). Among these, 78 (13%) had significant fibrosis. Patients with significant fibrosis had higher rates of type 2 diabetes (41% vs 21%, P < 0.001) and elevated levels of aspartate aminotransferase, alanine aminotransferase, hemoglobin A1c, Fibosis-4, aspartate-aminotransferase-to platelet-ratio index, and NAFLD fibrosis scores. They also exhibited higher visceral and subcutaneous fat. Binary logistic regression revealed type 2 diabetes and a visceral fat level of >15% as associated with significant liver fibrosis. Additionally, the DVF15 score, combining these factors, showed a modest area under the receiver operating characteristic curve of 0.664 (P < 0.001). Conclusion: Our study identified diabetes and high visceral fat as factors associated with significant liver fibrosis in MASLD patients. We recommend that visceral fat measurement using BIA be an essential part of MASLD evaluation. The presence of either diabetes or a visceral fat level of >15% should prompt clinicians to check for significant fibrosis in MASLD patients. Further research is warranted to validate our findings and evaluate the utility of the DVF15 score in larger cohorts and diverse populations.

The association of isocarbophos and isofenphos with different types of glucose metabolism: The role of inflammatory cells.

To investigate the associations between isocarbophos and isofenphos with impaired fasting glucose (IFG) and type 2 diabetes mellitus (T2DM), and to assess the mediation roles of inflammation cells. There were 2701 participants in the case-control study, including 896 patients with T2DM, 900 patients with IFG, 905 subjects with NGT. Plasma isocarbophos and isofenphos concentrations were measured using gas chromatography and triple quadrupole tandem mass spectrometry. Generalized linear models were used to calculate the relationships between plasma isofenphos and isocarbophos levels with inflammatory factor levels and T2DM. Inflammatory cell was used as mediators to estimate the mediating effects on the above associations. Isocarbophos and isofenphos were positively related with T2DM after adjusting for other factors. The odds ratio (95% confidence interval) (OR (95%CI)) for T2DM was 1.041 (1.015, 1.068) and for IFG was 1.066 (1.009, 1.127) per unit rise in ln-isocarbophos. The prevalence of T2DM increased by 6.4% for every 1 unit more of ln-isofenphos (OR (95% CI): 1.064 (1.041, 1.087)). Additionally, a 100% rise in ln-isocarbophos was linked to 3.3% higher ln-HOMA2IR and a 0.029 mmol/L higher glycosylated hemoglobin (HbA1c) (95% CI: 0.007, 0.051). While a 100% rise in ln-isofenphos was linked to increase in ln-HOMA2 and ln-HOMA2IR of 5.8% and 3.4%, respectively. Furthermore, white blood cell (WBC) and neutrophilic (NE) were found to be mediators in the relationship between isocarbophos and T2DM, and the corresponding proportions were 17.12% and 17.67%, respectively. Isofenphos and isocarbophos are associated with IFG and T2DM in the rural Chinese population, WBC and NE have a significant role in this relationship.

Evaluating the Causal Effect of Type 2 Diabetes on Alzheimer's Disease Using Large-Scale Genetic Data.

BACKGROUND: Alzheimer's disease (AD) has a high comorbidity with type 2 diabetes (T2D). However, there is still some controversy over whether T2D has a causal impact on AD at present. OBJECTIVES: We aimed to reveal whether T2D has a causal effect on AD using large-scale genetic data. METHODS: Firstly, we performed a primary two-sample Mendelian randomization (MR) analysis to assess the potential causal effects of T2D on AD. For this analysis, we used the largest available genome-wide association studies (GWAS) T2D (T2D1, including 80,154 cases and 853,816 controls) and AD (AD1, including 111,326 cases and 677,663 controls) datasets. Additionally, we performed a validation MR analysis using two largely overlapping-sample datasets from FinnGen, including T2D (T2D2, including 57,698 cases and 308,252 controls) and AD (AD2, including 13,393 cases and 363,884 controls). In all MR analyses, the inverse variance-weighted method was used as the primary analysis method, supplemented by the weighted-median and MR-Egger techniques. RESULTS: In the primary analysis, we found that T2D was not associated with the risk of AD (OR: 0.98, CI: 0.95-1.01, P=0.241). Similarly, no significant association was detected in the validation MR analysis (OR: 0.97, CI: 0.64-1.47, P=0.884). CONCLUSION: Our findings provide robust evidence that T2D does not have a causal impact on AD. Future studies need to further explore the effect of T2D on the non-AD components of the dementia phenotype.

Serum levels of the incretin-like peptide 26RFa are diminished in women living with obesity and diabetes and restored after sleeve gastrectomy: Results from the prospective pilot RFa-Ba-S study.

AIM: To investigate the evolution of the incretin-like peptide 26RFa in a prospective cohort of women living with obesity with or without type 2 diabetes (T2D) before and after sleeve gastrectomy (SG). METHODS: In this study, a total of 61 women were divided into three groups: women living with severe obesity without T2D (WlwOB group), women living with severe obesity and T2D (WlwOB-T2D group) and lean healthy volunteers (control group). Serum 26RFa concentrations were measured using a 26RFa enzyme-linked immunosorbent assay developed specifically for this study during meal tests before SG, and 30 and 180 days after SG. RESULTS: At baseline, serum 26RFa levels were reduced in the WlwOB (P < .05) and WlwOB-T2D (P < .01) groups compared with controls. In the WlwOB-T2D group, fasting 26RFa levels were found to increase throughout the entire follow-up period up to 6 months after the SG (P < .001). During the meal tests, serum 26RFa levels increased, especially in the WlwOB-T2D group at baseline. At the end of the follow-up, the profile of 26RFa concentrations obtained during the meal test in patients with severe obesity and T2D was similar to that of the controls. CONCLUSIONS: This prospective clinical study provides the first evidence that circulating 26RFa is altered mainly in WlwOB-T2D, and that these defects are partially reversed after SG.

[The Expression of TP53TG1, LINC00342, MALAT1, H19, and MEG3 Long Noncoding RNAs in Type 2 diabetes mellitus].

Type 2 diabetes is a complex and multifactorial metabolic disorder. The frequency of type 2 diabetes has dramatically increased worldwide. Long noncoding RNAs play a regulatory role in pathological processes of type 2 diabetes. The aim of the study was to analyze TP53TG1, LINC00342, MALAT1, H19, and MEG3 lncRNAs in patients with type 2 diabetes and metabolic parameters, as well as the risk of diabetic retinopathy. Participants included 51 patients with diabetes and 70 healthy individuals. The expression of the TP53TG1 and LINC00342 genes was significantly decreased in the patients with diabetes compared to healthy individuals. MALAT1 gene expression was higher in diabetes patients. H19 gene expression was increased in the patients with diabetic retinopathy compared patients without retinopathy. TP53TG1, LINC00342, and MEG3 expression was decreased in patients with diabetic retinopathy and MALAT1 expression was increased. H19 is positively correlated with triglyceride levels; TP53TG1 and LINC00342 are positively correlated with HbA1c levels and fasting glucose levels. MALAT1 is negatively correlated with HDL levels and positively correlated with LDL levels. A decrease in the expression level of TP53TG1 and LINC00342 and an increase in the level of MALAT1 in diabetes, as well as an association with glycemic control, indicate the role of the studied noncoding RNAs in the development of type 2 diabetes mellitus and retinopathy and can be considered as candidates for early diagnosis of type 2 diabetes.

Key biomarkers in type 2 diabetes patients: A systematic review.

Type 2 diabetes mellitus (T2DM) is not just a local health issue but a significant global health burden, affecting patient outcomes and clinical management worldwide. Despite the wealth of studies reporting T2DM biomarkers, there is an urgent need for a comparative review. This review aims to provide a comprehensive analysis based on the reported T2DM biomarkers and how these are linked with other conditions, such as inflammation and wound healing. A comparative review was conducted on 24 001 study participants, including 10 024 T2DM patients and 13 977 controls (CTL; age 30-90 years). Four main profiles were extracted and analysed from the clinical reports over the past 11 years: haematological (1084 cases vs. 1458 CTL), protein (6753 cases vs. 9613 CTL), cytokine (975 cases vs. 1350 CTL) and lipid (1212 cases vs. 1556 CTL). This review provides a detailed analysis of the haematological profile in T2DM patients, highlighting fundamental changes such as increased white blood cells and platelet counts, accompanied by decreases in red blood cell counts and iron absorption. In the serum protein profile, a reduction in albumin and anti-inflammatory cytokines was noted along with an increase in globulin levels and pro-inflammatory cytokines. Furthermore, changes in lipid profiles were discussed, specifically the decreases in high-density lipoprotein (HDL) and the increases in low-density lipoprotein (LDL) and triglycerides. Understanding the changes in these four biomarker profiles is essential for developing innovative strategies to create diagnostic and prognostic tools for diabetes management.

Efficacy of vitamin D supplementation on glycaemic control in type 2 diabetes: An updated systematic review and meta-analysis of randomized controlled trials.

AIM: To assess the effects of vitamin D interventions on glycaemic control in subjects with type 2 diabetes (T2D). METHODS: We searched PubMed, EMBASE, Web of Science and the Cochrane Library for relevant studies. Serum 25(OH)D, fasting blood glucose (FBG), HbA1c, fasting insulin and Homeostasis Model Assessment for Insulin Resistance (HOMA-IR) were analysed. RESULTS: We identified 39 randomized controlled trials involving 2982 subjects. Results showed a significant decline in the vitamin D group, as shown by the FBG weighted mean difference (WMD; -0.49 [95% confidence interval {CI}: -0.69 to -0.28] mmol/L), HbA1c (WMD -0.30% [95% CI: -0.43 to -0.18]), HOMA-IR (WMD -0.39 [95% CI -0.64 to -0.14]) and insulin (WMD -1.31 [95% CI: -2.06 to -0.56] µIU/mL). Subgroup analyses indicated that the effects of vitamin D supplementation on glycaemic control depend on the dosage and duration of supplementation, baseline 25(OH)D levels and the body mass index of patients with T2D. CONCLUSIONS: Vitamin D supplementation can significantly reduce serum FBG, HbA1c, HOMA-IR and fasting insulin levels in T2D patients; the effects were especially prominent when vitamin D was given in a short-term, high dosage to patients with a vitamin D deficiency, who were overweight, or had an HbA1c of 8% or higher at baseline. Our study suggests that vitamin D supplements can be recommended as complementary treatment for T2D patients.

Bioengineered Nanomedicines Targeting the Intestinal Fc Receptor Achieve the Improved Glucoregulatory Effect of Semaglutide in a Type 2 Diabetic Mice Model.

The oral administration of the glucagon-like peptide-1 analogue, semaglutide, remains a hurdle due to its limited bioavailability. Herein, neonatal Fc receptor (FcRn)-targeted nanoparticles (NPs) were designed to enhance the oral delivery of semaglutide. The nanocarriers were covalently linked to the FcRn-binding peptide FcBP or the affibody molecule ZFcRn that specifically binds to the human FcRn (hFcRn) in a pH-dependent manner. These FcRn-targeted ligands were selected over the endogenous ligands of the receptor (albumin and IgG) due to their smaller size and simpler structure, which could facilitate the transport of functionalized NPs through the tissues. The capacity of FcRn-targeted semaglutide-NPs in controlling the blood glucose levels was evaluated in an hFcRn transgenic mice model, where type 2 diabetes mellitus (T2DM) was induced via intraperitoneal injection of nicotinamide followed by streptozotocin. The encapsulation of semaglutide into FcRn-targeted NPs was translated in an improved glucoregulatory effect in T2DM-induced mice when compared to the oral free semaglutide or nontargeted NP groups, after daily oral administrations for 7 days. Notably, a similar glucose-lowering response was observed between both FcRn-targeted NPs and the subcutaneous semaglutide groups. An increase in insulin pancreatic content and a recovery in ß cell mass were visualized in the mice treated with FcRn-targeted semaglutide-NPs. The biodistribution of fluorescently labeled NPs through the gastrointestinal tract demonstrated that the nanosystems targeting the hFcRn are retained longer in the ileum and colorectum, where the expression of FcRn is more prevalent, than nontargeted NPs. Therefore, FcRn-targeted nanocarriers proved to be an effective platform for improving the pharmacological effect of semaglutide in a T2DM-induced mice model.

Impact of diverse aerobic exercise plans on glycemic control, lipid levels, and functional activity in stroke patients with type 2 diabetes mellitus.

Aims: This study aimed to assess the effects of Low-to-Moderate Intensity Continuous Training (LMICT), Moderate-Intensity Interval Training (MIIT), and Reduced-Exertion High-Intensity Training (REHIT) on blood glucose regulation, functional recovery, and lipid levels in individuals who have experienced a stroke and are diagnosed with Type 2 Diabetes Mellitus (T2DM). Methods: Forty-two T2DM stroke patients were randomly allocated to four groups: LMICT, MIIT, REHIT, and a control group (CON). Participants continuously monitored their blood glucose levels throughout the intervention using continuous glucose monitoring (CGM) devices. The study comprised two exercise intervention cycles: the first lasting from Day 3 to Day 14 and the second from Day 15 to Day 28, with the initial two days serving as contrasting periods. Primary outcomes encompassed CGM-derived blood glucose measurements, the Barthel Index (BI), Fugl-Meyer Assessment lower-extremity subscale (FMA-LE), and alterations in triglycerides (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-c), and low-density lipoprotein cholesterol (LDL-c). Results: Compared with the CON, the MIIT group showed significant improvements in mean glucose (MG), glucose standard deviation (SD), time above range (TAR), and time in range (TIR). The REHIT group exhibited significantly reduced time below range (TBR), glucose SD, and coefficient of variation (CV). Regarding lipid levels, although the REHIT group achieved a significant reduction in TG levels compared with the CON, the overall effects of LMICT, MIIT, and REHIT on lipid profiles were relatively modest. Concerning functional recovery, the REHIT group significantly improved the BI and FMA-LE. Conclusion: Although the short-term quantitative impact of exercise on lipid levels may be limited, both REHIT and MIIT significantly improved glycemic management and reduced glucose variability in post-stroke patients with Type 2 Diabetes Mellitus. Additionally, REHIT notably enhanced functional recovery.

Exploring the clinical effectiveness of glucagon-like peptide-1 receptor agonists in managing cardiovascular complications: an updated comprehensive review and future directives.

The possible cardiovascular advantages of glucagon-like peptide-1 receptor agonists (GLP-1RAs), a class of drugs predominantly used to treat type 2 diabetes (T2D), have garnered increasing attention in recent years. Clinical trials have looked into the possibility that GLP-1RAs have extra cardioprotective benefits in addition to their ability to manage T2D, demonstrating significant major adverse cardiovascular events (MACE) reduction and a favorable safety profile. GLP-1 RAs improve cardiovascular outcomes, especially in those with existing cardiovascular disease. MACE has been steadily declining with this class of drugs, which results in a noticeable rise in cardiovascular outcome trials (CVOTs). GLP-1 RAs have a variety of impacts on the cardiovascular system beyond their function in glycemic control. They offer direct cardioprotection, vasodilation, promotion of salt excretion, reduction of weight, improved lipid profile, and anti-inflammatory qualities through a variety of mechanisms. Thus, this review focuses on GLP-1RAs, its mechanism of action, its clinical effectiveness in CVOTs, the mechanism behind its cardiovascular benefits, its potential role in heart failure, cardiovascular outcomes, its underutilization, and future directives. In conclusion, GLP-1 RAs shows potential in controlling T2D while also lowering cardiovascular risk, but warrants further study into long-term results and real-world data to optimize treatment regimens, ultimately increasing patient outcomes and lowering the burden of cardiovascular disease in T2D populations.

A nutrition-focused review of the interventions in US-living Latino communities with type II diabetes.

Type 2 diabetes (T2D) is a chronic, debilitating disease that disproportionally affects the Hispanic/Latino community residing in the United States. Optimal nutrition therapy is fundamental to the proper management of T2D and must be culturally adapted to facilitate permanent behavior change in this population. This review selected and assessed the nutrition components of interventions aimed to improve T2D outcomes in US-based Latinos/Hispanics, published from 2002 to 2023. An overview of the participant characteristics, nutrition intervention, and dietary assessment and outcomes is included. Nutrition interventions in this community benefit from the inclusion of bicultural registered dietitian nutritionist (RDNs) to assure the counseling team promotes culturally tailored nutrition recommendations based on current dietary guidelines. Nutrition assessment and outcomes should be captured with the use of validated dietary assessment tools and dietary quality indices appropriate to their target population. Standardizing these practices will facilitate intervention comparability and replicability and ultimately better target the needs of this community.

Association between bone microarchitecture and sarcopenia in postmenopausal women with type 2 diabetes.

Bone microarchitecture, as assessed using high-resolution peripheral quantitative computed tomography, is adversely affected in postmenopausal women with type 2 diabetes mellitus having sarcopenia/sarcopenic obesity while areal bone mineral density does not differ between those with and without sarcopenia. PURPOSE: Type 2 diabetes (T2D) increases the risk of sarcopenia, which independently contributes to bone fragility. We aimed to explore the association between sarcopenia/sarcopenic obesity and bone quality using second-generation high-resolution peripheral quantitative computed tomography (HR-pQCT) in T2D. METHODS: We analyzed the baseline participant characteristics of an ongoing randomized clinical pilot trial (CTRI/2022/02/039978). Postmenopausal women (≥ 50 years) with T2D and high risk of fragility fractures were included. Areal BMD (aBMD), trabecular bone score (TBS), and body composition were measured using DXA. Bone microarchitecture was assessed at distal radius/distal tibia using HR-pQCT. Muscle strength was estimated using dominant handgrip strength (HGS). Sarcopenia was defined as low HGS (< 18.0 kg) and low appendicular skeletal muscle index (ASMI) (< 4.61 kg/m2). Probable sarcopenia was defined as low HGS with normal ASMI. Sarcopenic obesity was classified as co-existence of sarcopenia and obesity (BMI ≥ 25.0 kg/m2). RESULTS: We recruited 129 postmenopausal women (mean age 64.2 ± 6.7 years). Participants were categorized into four mutually exclusive groups: group A (normal HGS and ASMI, n = 17), group B (probable sarcopenia, n = 77), group C (non-obese sarcopenia, n = 18), and group D (obese sarcopenia, n = 18). The four groups did not differ significantly with regard to baseline characteristics, fracture prevalence, HbA1c, aBMD, and TBS. However, HR-pQCT-derived volumetric BMD and cortical/trabecular microarchitecture were significantly poorer in group C/group D than in group A/group B. CONCLUSIONS: Bone quality rather than bone density (quantity) is adversely affected in T2D postmenopausal women with sarcopenia/sarcopenic obesity, which could increase the fracture risk in this patient sub-population.

Do ketone supplements regulate islet hormone secretion?

Ketone supplementation has been gaining interest in improving health and treating some diseases, such as diabetes. However, the mechanism of action of how these ketone supplements work is not fully understood. In a recent paper, Banerjee et al. (2024) showed that physiological concentrations of ßHB can affect hormone secretion and signalling within pancreatic islets. They showed that acute treatment with ßHB increases insulin secretion and decreases glucagon secretion at physiological glucose concentrations. Their studies also suggest chronic ßHB treatment may protect human islet cells from cytokine-induced cell death. Although more work is needed, it is possible that physiological concentrations of ßHB may influence hormone secretion and signalling within islets.

Individual and combined effects of muscle strength and visceral adiposity on incident prediabetes and type 2 diabetes in a longitudinal cohort of midlife Asian women.

AIM: To investigate the independent and combined effects of muscle strength and visceral adiposity on prediabetes and type 2 diabetes incidence among midlife women. MATERIALS AND METHODS: In this prospective study of midlife women (mean age 56.4 years), visceral adiposity, defined as visceral adipose tissue (VAT) >131 cm2 measured by dual energy X-ray absorptiometry, and poor combined muscle strength, defined as handgrip strength <18 kg and/or five-time repeated chair stand test performance ≥12 s, were determined at baseline between 2014 and 2016. After 6.6 years, the effects of VAT and muscle strength on risk of incident prediabetes (fasting blood glucose 5.6-6.9 mmol/L) and type 2 diabetes (fasting blood glucose levels ≥7 mmol/L, medication use, or physician diagnosis) were examined using modified Poisson regression analysis. RESULTS: Among the 733 initially normoglycaemic participants, 150 (20.5%) developed prediabetes or type 2 diabetes. Women with both poor combined muscle strength and high VAT had the highest risk for both prediabetes and type 2 diabetes (adjusted relative risk [aRR] 2.63, 95% confidence interval [CI] 1.81-3.82). In comparison, high VAT alone increased risk by 1.78-fold (95% CI 1.12-2.84). Stratification analyses showed that among women with low muscle strength, high VAT demonstrated increased risks of prediabetes and type 2 diabetes (aRR 2.84, 95% CI 1.95-4.14) compared to those with normal strength (aRR 1.66, 95% CI 1.04-2.65). CONCLUSIONS: Low combined muscle strength with high VAT poses a greater risk for the development of prediabetes and type 2 diabetes than high VAT alone. Muscle strengthening should be promoted alongside weight loss in diabetes prevention.

Type 2 diabetes mellitus and neurodegenerative disorders: The mitochondrial connection.

The incidence of type 2 diabetes mellitus (T2DM) has increased in our society in recent decades as the population ages, and this trend is not expected to revert. This is the same for the incidence of the main neurodegenerative disorders, including the two most common ones, which are, Alzheimer's and Parkinson's disease. Currently, no pharmacological therapies have been developed to revert or cure any of these pathologies. Interestingly, in recent years, an increased number of studies have shown a high co-morbidity between T2DM and neurodegeneration, as well as some common molecular pathways that are affected in both types of diseases. For example, while the etiopathology of T2DM and neurodegenerative disorders is highly complex, mitochondrial dysfunction has been broadly described in the early steps of both diseases; accordingly, this dysfunction has emerged as a plausible molecular link between them. In fact, the prominent role played by mitochondria in the mammalian metabolism of glucose places the physiology of the organelle in a central position to regulate many cellular processes that are affected in both T2DM and neurodegenerative disorders. In this collaborative review, we critically describe the relationship between T2DM and neurodegeneration; making a special emphasis on the mitochondrial mechanisms that could link these diseases. A better understanding of the role of mitochondria on the etiopathology of T2DM and neurodegeneration could pave the way for the development of new pharmacological therapies focused on the regulation of the physiology of the organelle. These therapies could, ultimately, contribute to increase healthspan.

Associations between polychlorinated biphenyls and cancer risk among type 2 diabetes: The modifying effects of lifestyle.

A growing percentage of diabetes-related deaths has been attributed to cancer, with environmental factors playing important contributions. Thus, we studied the potential relationship between endocrine disruptors polychlorinated biphenyls (PCBs) and cancer risk in diabetes. We aimed to evaluate the association between serum seven indicator-PCB (PCB-28/52/101/118/138/153/180) levels and incident cancer, and further explore the possible modifying role of lifestyle. A total of 2806 type 2 diabetes mellitus (T2DM) cases were included from the Dongfeng-Tongji cohort at the baseline in 2008 and tracked until December 2018, and 320 incident cancers were identified during about 10-year follow-up. Cox proportional hazards models and competing risk regression models were used to reveal associations of baseline concentrations of PCBs with total cancer and specific cancer, respectively. Lifestyle score was determined by body mass index, waist circumference, physical activity, smoking, alcohol drinking, and diet. Each interquartile range (IQR) increment of non-dioxin-like PCBs (NDL-PCBs) generated an 8%-30% increase in cancer incidence. Individuals in the highest quartile for PCB-52, PCB-101, PCB-138, and lowly chlorinated PCBs had 1.44- to 1.68-fold higher cancer risk compared to those in the lowest quartile. Restricted cubic spline analyses and the quantile g-computation model showed similar results. Significant interactions were found between PCBs and fasting blood glucose or simplified insulin resistance assessment indicators. NDL-PCBs were positively and significantly associated with gastrointestinal cancer and respiratory cancer, especially with liver cancer, colorectal cancer, and lung cancer. Higher PCBs showed a significant increase in total cancer risk among participants with an unhealthy lifestyle, however, no associations were observed in those with a relatively healthy lifestyle (Pinteraction < 0.05). Our findings indicated an increased cancer risk associated with NDL-PCBs, highlighted the role of a healthy lifestyle in potentially reducing adverse impact, and provided preliminary data for environmental and public health interventions to alleviate the risk of cancer among diabetes.

Association of dietary antioxidant indices with kidney function indicators in patients with type 2 diabetes: a cross-sectional study.

This cross-sectional study investigated the relationship between dietary antioxidant indices and kidney function indicators in 240 outpatient adults with type 2 diabetes. Dietary intake was assessed using three 24-h dietary recalls. Dietary total antioxidant capacity (DTAC), dietary antioxidant index (DAI), and dietary antioxidant quality score (DAQS) were obtained. Indicators of kidney function, including serum creatinine, urea, blood urea nitrogen (BUN), and glomerular filtration rate (GFR), were extracted from medical records. After adjustment, the highest DAI tertile had lower serum creatinine (0.98 ± 0.27 vs 1.03 ± 0.32 mg/dL, P < 0.001), reduced urea (30.97 ± 8.75 vs 34.07 ± 14.45 mg/dL, P = 0.005), and higher GFR (85.16 ± 29.43 vs 74.16 ± 22.18 ml/min per 1·73 m2, P < 0.001) compared to the lowest tertile. The results of logistic regression analysis indicated a borderline significant inverse association of serum urea > 20 mg/dl with DTAC (odds ratio (OR):0.28; 95% CI: 0.07-1.09; Ptrend = 0.06). Multivariable linear regression analysis revealed a significant aligned correlation between DAQs and GFR (ß: 0.20; P-value: 0.005) and a marginally significant direct relationship between DAI and GFR (ß: 0.14; P-value: 0.06). However, no significant association was observed for DTAC with GFR (ß:-0.02; P-value: 0.80). Diets with higher antioxidant capacity may be linked to improved kidney function in type 2 diabetes but our results did not support this strongly.

Exploring the association of social connections and food security among adults with uncontrolled type 2 diabetes: a population-based study.

BACKGROUND: Primary health care professionals are held accountable for various quality measures in the treatment of patients with chronic diseases such as diabetes. Uncontrolled type 2 diabetes (T2D) remains a considerable health problem; thus, further studying patients with this condition is important for delivering effective interventions. Social determinants of health (SDoH) have been shown to affect various aspects of diabetes care in different subpopulations. We studied the association of SDoH with uncontrolled T2D in a population of adult primary care patients. METHODS: We retrospectively searched our electronic health record for adult patients (≥18 years) with a diagnosis of T2D and a hemoglobin A1c (HbA1c) level of 8% or higher. Patients were empaneled to 2 primary care clinic sites between January 1, 2021, and January 31, 2022. Patients were grouped by HbA1c level to stratify patients according to the extent of uncontrolled T2D. Patient characteristics were compared among groups. Unadjusted and adjusted multinomial logistic regression analysis was used to estimate the odds of various SDoH factors among patient groups with different levels of uncontrolled T2D. RESULTS: The study cohort included 1,596 patients. Most patients were White (79%), and the median age was 58.8 years. The median HbA1c level was 8.9%, and approximately 68% of patients were obese (body mass index [BMI] ≥30). When the study population was grouped by HbA1c level (8% to < 9% [n = 806], ≥9% to < 12% [n = 684], and ≥12% [n = 106]), significant differences among groups were observed in age group (P < .001), marital status (P < .001), race (P < .001), ethnicity (P = .001), and BMI category (P = .01). In groups with higher HbA1c levels, we noticed a higher percentage of patients who were aged 51 to 65 years or single. Among patients with uncontrolled HbA1c levels, more patients were obese than overweight. Patients in the intermediate HbA1c group had increased odds of food insecurity and some decreased social connections, even after adjusting for age, sex, race, ethnicity, and marital status. CONCLUSIONS: Among patients with uncontrolled T2D, higher HbA1c levels were associated with decreased social connections and increased food insecurity. Our findings provide insight into the role of these SDoH in managing T2D and have important implications for primary care practice.

Development and Validation of a Nocturnal Hypoglycaemia Risk Model for Patients With Type 2 Diabetes Mellitus.

AIM: To develop and test different machine learning algorithms for predicting nocturnal hypoglycaemia in patients with type 2 diabetes mellitus. DESIGN: A retrospective study. METHODS: We collected data from dynamic blood glucose monitoring of patients with T2DM admitted to the Department of Endocrinology and Metabolism at a hospital in Shanghai, China, from November 2020 to January 2022. Patients undergone the continuous glucose monitoring (CGM) for ≥ 24 h were included in this study. Logistic regression, random forest and light gradient boosting machine algorithms were employed, and the models were validated and compared using AUC, accuracy, specificity, recall rate, precision, F1 score and the Kolmogorov-Smirnov test. RESULTS: A total of 4015 continuous glucose-monitoring data points from 440 patients were included, and 28 variables were selected to build the risk prediction model. The 440 patients had an average age of 62.7 years. Approximately 48.2% of the patients were female and 51.8% were male. Nocturnal hypoglycaemia appeared in 573 (14.30%) of 4015 continuous glucose monitoring data. The light gradient boosting machine model demonstrated the highest predictive performances: AUC (0.869), specificity (0.802), accuracy (0.801), precision (0.409), recall rate (0.797), F1 score (0.255) and Kolmogorov (0.603). The selected predictive factors included time below the target glucose range, duration of diabetes, insulin use before bed and dynamic blood glucose monitoring parameters from the previous day. PATIENT OR PUBLIC CONTRIBUTION: No Patient or Public Contribution.

Altered Subcortical Brain Volume and Cortical Thickness Related to Insulin Resistance in Type 2 Diabetes Mellitus.

PURPOSE: The objective of this study is to examine the alterations in subcortical brain volume and cortical thickness among individuals diagnosed with Type 2 diabetes mellitus (T2DM) through the application of morphometry techniques and, additionally, to investigate the potential association between these modifications and insulin resistance (IR). MATERIALS AND METHODS: The present cross-sectional study comprised a total of 121 participants (n = 48 with healthy controls [HCs] and n = 73 with T2DM) who were recruited and underwent a battery of cognitive testing and structural magnetic resonance imaging (MRI). FreeSurfer was used to process the MRI data. Analysis of covariance compared discrepancies in cortical thickness and subcortical brain volume between T2DM and HCs, adjusting for the potential confounding effects of gender, age, education, and body mass index (BMI). Exploratory partial correlations investigated links between IR and brain structure in T2DM participants. RESULTS: Compared with HCs, individuals with T2DM demonstrated a cortical thickness decrease in the right caudal middle frontal gyrus, right pars opercularis, left precentral gyrus, and bilateral superior frontal gyrus. Furthermore, this study for T2DM found that the severity of IR was inversely related to the volume of the left putamen and left hippocampus, as well as the thickness of the left pars orbitalis, left pericalcarine, right entorhinal area, and right rostral anterior cingulate gyrus. CONCLUSION: The evidence for structural brain changes in T2DM was observed, and alterations in cortical thickness were concentrated in the frontal lobes. Correlations between IR and frontal cortical thinning may serve as a potential neuroimaging marker of T2DM and lead to various diabetes-related brain complications.