Markers Of Glucose Metabolism Research Articles

Evaluating the prognostic role of glucose-to-lymphocyte ratio in patients with metastatic renal cell carcinoma treated with tyrosine kinase inhibitors in first line: a study by the Turkish Oncology Group Kidney Cancer Consortium (TKCC).

Identifying prognostic indicators for risk stratification in metastatic renal cell carcinoma (mRCC) is crucial for optimizing treatment strategies and follow-up plans. This study aims to investigate the prognostic role of the glucose-to-lymphocyte ratio (GLR) in patients with mRCC receiving tyrosine kinase inhibitors (TKIs) as first-line therapy. A retrospective cohort study was conducted using data from the Turkish Oncology Group Kidney Cancer Consortium Database. GLR was calculated by dividing the fasting glucose (mmol/L) by the lymphocyte count (×109/L). We categorized patients into two categories based on their median GLR level. The analysis included a total of 598 patients. We found that progression-free survival (PFS) was significantly longer in the GLR-low group, with a median PFS of 15.05 months (95% CI 12.7-17.4) compared to 7.79 months (95% CI 6.6-9.0) in the GLR-high group (p < 0.001). Multivariate analysis identified GLR as an independent risk factor for poor PFS (HR 1.39, 95% CI 1.12-1.72; p = 0.003). Overall survival (OS) was also significantly longer in the GLR-low group, with a median OS of 38.47 months (95% CI, 30.9-46.0) compared to 24.15 months (95% CI 18.0-30.2) in the GLR-high group (p = 0.001). GLR was an independent predictor for OS in multivariate analysis (HR 1.45, 95% CI 1.12-1.86; p = 0.004). The GLR can be a valuable prognostic marker for glucose metabolism and systemic inflammatory status in this patient population. Our research highlights the potential prognostic value of GLR in patients with mRCC receiving TKIs, indicating its potential as a useful tool for clinical decision-making.

The Evaluation of Biochemical Parameters in Positive COVID-19 RealTime PCR Patients: A Retrospective Study

Coronavirus, a member of the beta coronavirus family, encompasses a range of illnesses from common colds to severe disorders. SARS-CoV-2, transmitted mainly through respiratory droplets that are generated by a patient who is sneezing, coughing and talking, caused the global pandemic COVID-19 in 2020. The virus primarily targets the respiratory system especially in the lung cell, leading to diverse symptoms and severe consequences. This study was carried out in the COVID-19 Isolation Centre in Mukalla City, Yemen, to evaluate biochemical tests in COVID-19 patients. In the retrospective single-centre study on 116 COVID-19 patients, some of biochemical Analysed Parameters were glucose, Liver function tests, renal function tests, lipid profile, and proinflammatory markers; convenience sampling based on existing records for socio-demographics, medical history, and biochemistry were analysed by using a spectrophotometry and Chemiluminescent immunoassay analyser. used SPSS version 25 to analyse data. Most COVID-19 patients in Mukalla City (91.4 % of those over 46 years old) have common symptoms such as fever, cough, and respiratory problems. The study found links between chronic health disorders (hypertension 96.6 %, diabetes mellitus 94.8 %) and greater vulnerability to COVID-19. Blood glucose levels substantially impact COVID-19 occurrences (p 0.0001). Some liver function tests are associated with COVID-19 (total protein, albumin, LDH, and GGT) (p = 0.044, 0.010, 0.0001, and 0.0001, respectively). Urea and creatinine levels imply renal function and their significant association (p=0.001 for both), whereas uric acid had no significant association with COVID-19 (p = 0.134). However, lipid profile tests lack statistical significance; they do identify trends. Proinflammatory markers CRP and ferritin strongly correlate with positive COVID-19 patients (p=0.0001 for both). In conclusion, COVID-19 significantly affects glucose metabolism, liver function, renal dynamics, and inflammatory markers, necessitating vigilant monitoring for clinical care and informing future research.

Dynamics of Glycemic Status and Glucose Metabolism Markers 12 Months After Coronary Artery Bypass Grafting and Their Relationship with the Annual Prognosis of Patients

Dynamics of Glycemic Status and Glucose Metabolism Markers 12 Months After Coronary Artery Bypass Grafting and Their Relationship with the Annual Prognosis of Patients

Impact of bedroom light exposure on glucose metabolic markers and the role of circadian-dependent meal timing: A population-based cross-sectional study.

Light at night (LAN) has become a global concern. However, little is known about the effects of bedroom LAN exposure on glucose metabolism markers. We aimed to explore the association between intensity and duration of bedroom LAN exposure with glucose metabolism markers, and the role of circadian-dependent meal timing in these associations. Real-ambient bedroom LAN exposure was measured using a portable illuminance meter for two consecutive days. Seven consecutive days of sleep time and 24-h dietary records were assessed by wrist-worn accelerometer and mobile phone photos, respectively. Circadian-dependent meal timing, including the timing of meal relative to clock time and sleep time, was calculated from 24-h dietary records and sleep data. The mean age of participants was 18.7 years, and 32.8 % were male. Per SD lx increase of bedroom LANavg was associated with 1.75 μU/mL-increase in INS (95 %CI: 0.10, 2.50), 0.61 unit-increase in HOMA-IR (95 %CI: 0.43, 0.79), and 0.09 unit-increase in TyG (95 %CI: 0.04, 0.15); per SD min increase of bedroom LAN3 was associated with 1.61 μU/mL-increase in INS (95 %CI: 0.84, 2.37), 0.48 unit-increase in HOMA-IR (95 %CI: 0.29, 0.67), and 0.07 unit-increase in TyG (95 %CI: 0.01, 0.13). Nevertheless, these associations were found to be significant in later circadian-dependent meal timing group while weaker or not significant in earlier circadian-dependent meal timing group (time of first meal ≤ 9:00, time of last meal ≤ 19:00, first meal - sleep end ≤ 2 h, and sleep onset - last meal ≥ 5 h). Overall, bedroom LAN exposure was associated with impaired glucose metabolism markers among young adults. Importantly, circadian-dependent meal timing may have potentially moderate effects on these associations. Keeping bedroom darkness at night and adhering to early eating pattern may be important public health strategies to reduce the risk of glucose metabolism disorders.

Indicators of Glucose Metabolism in Children and Adolescents Characterized as Having “Metabolically Healthy” and “Metabolically Unhealthy” Obesity

Background/Objectives: Some individuals with obesity may exhibit fewer metabolic disturbances and face a lower long-term risk of complications; however, the existence of this so-called “metabolically healthy obesity” (MHO) compared to “metabolically unhealthy obesity” (MUO) remains controversial. We hypothesized that children with MHO might have a more favorable profile than children with MUO. Markers of glucose metabolism and insulin sensitivity were compared between children and adolescents diagnosed with MHO and MUO. Methods: This study recruited prospectively 104 children and adolescents (aged 6–16 years, 47 boys) with obesity. All participants underwent an oral glucose tolerance test (OGTT), and a comparative analysis was performed on HOMA-IR, QUICKI, insulin sensitivity index (ISI), insulinogenic index (IGI), disposition index (DI), and oral disposition index (oDI). Glucose metabolism indices were compared in these subgroups according to pubertal status. Results: Forty-seven children (45.2%) were diagnosed with MHO. The whole-body ISI differed significantly between the MHO and MUO groups (4.02 vs. 2.7, p &lt; 0.01). The IGI was statistically lower in the MHO group compared to MUO (1.26 vs. 1.54, p &lt; 0.01), while neither the DI nor the oDI differed significantly. A higher ISI (4.5 vs. 3.9, p &lt; 0.01) was observed in prepubertal MHO individuals compared to MHO adolescents. Conclusions: Children classified as MHO according to the more recent criteria exhibit a more favorable metabolic profile than those with MUO. However, a completely healthy profile was not demonstrated in the MHO group, as many crucial metabolic profile parameters were comparable to those observed in the MUO group. The findings of this study indicate that all children with obesity, irrespective of whether they are categorized as having MUO or MHO, necessitate close monitoring.

Involvement of circulating microRNAs in the pathogenesis of atherosclerosis in young patients with obesity.

Obesity is considered an important factor contributing to the development of atherosclerosis. Inflammation plays a key role in endothelial dysfunction (ED), an initial stage of the atherosclerotic process. Several microRNAs (miRNAs) may play an important role in the inflammatory process, but there is a lack of information about their participation in the early stages of atherosclerosis development in patients with obesity. We aimed to assess the relations between plasma concentration of selected miRNAs, ED evaluated by reactive hyperemia index (RHI), inflammatory markers and other factors involved in the pathogenesis of atherosclerosis in adolescents and young adults with obesity. Participants (30 males, 30 females; aged 15 25 years) were divided into two groups: those with overweight/obesity (OW/O) (20 males, 20 females) and controls (C) (10 males, 10 females). The plasma concentrations of inflammatory markers, cytokines, adipocytokines, markers of lipid profile and glucose metabolism and selected miRNAs (miR 92, 126, -146a, -155) were analyzed. No significant differences in any of the miRNAs were found between the groups. MiR-146a correlated positively with RHI. Dividing the group by sex showed more significant associations between miRNA and analyzed parameters (IL-6, fasting glycemia) in men. Several observed correlations indicate a potential role of miRNAs in inflammation, the atherosclerotic process and glycemic control, primarily in male subjects with obesity. The relatively low number of observed associations between assessed parameters related to obesity and the pathogenesis of its complications could be attributed to the early stage of the atherosclerotic process in young subjects with obesity, where only subtle abnormalities are expectedly found. Key words Endothelial dysfunction, Atherosclerosis, Obesity, MicroRNA, Reactive hyperemia index.

BETA CELL DYSFUNCTION OCCURS INDEPENDENTLY OF INSULITIS IN TYPE 1 DIABETES PATHOGENESIS.

During type 1 diabetes (T1D) progression, beta cells become dysfunctional and exhibit reduced first-phase insulin release. While this period of beta cell dysfunction is well established, its cause and underlying mechanism remain unknown. To address this knowledge gap, live human pancreas tissue slices were prepared from autoantibody-negative organ donors without diabetes (ND), donors positive for one or more islet autoantibodies (AAb+), and donors with T1D within 0-4 years of diagnosis (T1D+). Dynamic imaging and physiological secretion studies were conducted to assess the extent and impact of T cell infiltration on beta cell function through immunolabeling, Ca2+ imaging, and perifusion assays for insulin secretion. Beta cells were identified in living slices by ENTPD3 cell surface staining. Beta cells from both ND and AAb+ donors exhibited normal cytosolic Ca2+ mobilization in response to high glucose and KCl. Beta cells from donors with T1D had significantly diminished Ca2+ responses to high glucose but preserved responses to KCl. In T1D, glucose responsiveness was impaired in both T cell-infiltrated and non-infiltrated insulin positive islets, supporting the concept that beta cell dysfunction is independent of close spatial association between beta cells and T cells. Fixed tissue staining and gene expression profiling of laser-capture microdissected islets revealed significant decreases in markers of glucose metabolism to ATP in beta cells from donors with T1D but no changes in endoplasmic reticulum (ER) stress markers. From these data, we posit that functional defects occur in beta cells during T1D pathogenesis independent of local T cell infiltration and beta cell destruction. Additionally, these beta cell metabolic defects contribute to the clinical manifestation of dysglycemia at T1D diagnosis despite a remaining mass of beta cells.

Probiotics: A Potential Strategy for Preventing and Managing Cardiovascular Disease.

Probiotics are gaining recognition as a viable strategy for mitigating cardiovascular risk factors. Specifically, recent studies highlight their potential benefits in managing cholesterol levels, blood pressure, and inflammation, which are critical components in the prevention of cardiovascular diseases (CVD). This comprehensive review aims to elucidate the impact of probiotic consumption on major cardiovascular risk factors, including individuals with hypertension, type II diabetes mellitus, metabolic syndrome, hypercholesterolemia, and in secondary prevention in coronary artery disease. Scientific evidence based on human studies suggests that probiotic consumption is associated with positive effects on anthropometric measures, inflammation markers, blood pressure, glucose metabolism markers, lipid profiles, and endothelial function. However, these findings should be interpreted pragmatically and acknowledge the significant variability in results. This variability may be attributed to factors such as probiotic composition (single strain or multiple strains), the characteristics of the delivery matrix (food, capsules, and sachets), the duration of the intervention, the dosage regimen, and baseline health profiles of the participants. Incorporating probiotics as part of a comprehensive and healthy lifestyle approach can be considered a feasible strategy for both the prevention and management of CVD. However, further research is needed on factors influencing the effect of probiotics, such as: (i) optimal probiotic strain(s), (ii) appropriate dosage, (iii) duration of treatment, (iv) optimal delivery vehicle, and (v) sex-specific differences.

Relationship Between Hepatic Iron Concentration and Glycemic Metabolism, Prediabetes, and Type 2 Diabetes: A Systematic Review.

Emerging research has suggested a potential link between high iron levels, indicated by serum ferritin levels, and the development of type 2 diabetes (T2D). However, the role of hepatic iron concentration (HIC) on T2D development and progression is not well understood. This study aims to systematically review the literature on HIC and/or the degree of hepatic iron overload (HIO) in individuals with prediabetes and/or diagnosed T2D, and to analyze associations between HIC and markers of glucose metabolism. The databases Medline, PubMed, Embase, CINAHL, and Web of Knowledge were searched for studies published in English from 1999 to March 2024. This review followed the Preferred Items for Systematic Reviews and Meta-Analyses (PRISMA) checklist. Data were extracted following the established eligibility criteria. Study characteristics and biomarkers related to prediabetes, T2D, and HIO were extracted. The risk of bias was analyzed using the Newcastle-Ottawa Scale. Data were stratified by the exposure and analyzed in subgroups according to the outcome. Data regarding the HIC values in controls, individuals with prediabetes, and individuals with T2D and the association estimates between HIC or HIO and markers of glycemic metabolism, prediabetes, or T2D were extracted. A total of 12 studies were identified, and data from 4110 individuals were analyzed. HIO was not consistently observed in prediabetic/T2D populations; however, elevated HIC was frequently observed in prediabetic and T2D individuals, and was associated with the disruption of certain glycemic markers in some cases. The extent of iron overload, as indicated by hepatic iron load, varied among the prediabetic and T2D populations studied. Further research is needed to understand the distribution and regulation of iron in T2D pathology.

Acupoint thread-embedding at fat layer for abdominal obesity: a randomized controlled trial

To observe the clinical efficacy of acupoint thread-embedding at fat layer for abdominal obesity and its effects on glucose and lipid metabolism. Ninety-six patients with abdominal obesity were randomly divided into an acupoint embedding group (48 cases, 3 cases dropped out) and a sham embedding group (48 cases, 3 cases dropped out). Both groups received lifestyle interventions as basic treatment. The acupoint embedding group underwent thread-embedding at Zhongwan (CV 12), Qihai (CV 6), Guanyuan (CV 4), and bilateral Liangmen (ST 21), Fenglong (ST 40), and Pishu (BL 20), with the thread implanted in the fat layer. The sham embedding group followed the same acupoint selection and procedure but without catgut implantation. Both groups were treated once every two weeks for 12 weeks, for a total of six treatments. Waist circumference, body weight, body mass index (BMI), waist-to-hip ratio (WHR), and waist-to-height ratio (WHtR) were measured, and appetite was assessed using the visual analogue scale (VAS) before and after treatment and at 12 weeks after treatment completion (follow-up) in the two groups. Visceral fat area (VFA) and subcutaneous fat area (SFA) at abdomen were measured, and blood glucose and lipid metabolism markers, including fasting blood glucose (FBG), fasting insulin (FINS), homeostasis model assessment of insulin resistance (HOMA-IR) index, total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), leptin, tumor necrosis factor-α(TNF-α), and interleukin-6 (IL-6), were also tested before and after treatment in the two groups. Clinical efficacy was evaluated two weeks after treatment completion. After treatment and at follow-up, the waist circumference, body weight, BMI, WHR, WHtR, and appetite VAS scores in the acupoint embedding group were decreased compared to those before treatment (P<0.01). In the sham embedding group, waist circumference, body weight, BMI, WHtR, and appetite VAS score were also reduced after treatment compared to those before treatment (P<0.01). Except for body weight after treatment, the acupoint embedding group showed lower waist circumference, body weight, BMI, WHR, and WHtR values after treatment and at follow-up compared to the sham embedding group (P<0.01, P<0.05). Additionally, the appetite VAS score in the acupoint embedding group was lower than that in the sham embedding group after treatment (P<0.01). Both groups showed a reduction in abdominal VFA and SFA after treatment compared to those before treatment (P<0.01, P<0.05). In the acupoint embedding group, serum FBG, FINS, HOMA-IR index, TC, TG, LDL-C, leptin, TNF-α, and IL-6 levels were decreased compared to those before treatment (P<0.01), while HDL-C level was increased (P<0.01). In the sham embedding group, serum FBG and HOMA-IR index were decreased compared to those before treatment (P<0.01, P<0.05). After treatment, the abdominal SFA in the acupoint embedding group was lower than that in the sham embedding group (P<0.01). Additionally, the acupoint embedding group had lower levels of serum FINS, HOMA-IR index, TC, LDL-C, leptin, TNF-α, and IL-6 compared to the sham embedding group (P<0.05, P<0.01). The total effective rate in the acupoint embedding group was 82.2% (37/45), which was significantly higher than 15.6% (7/45) in the sham embedding group (P<0.01). The acupoint catgut embedding at fat layer could effectively reduce the obesity severity in patients with abdominal obesity, decrease abdominal fat accumulation, suppress appetite, improve glucose and lipid metabolism, reduce inflammatory responses, and has a sustained effect.

HOMA-beta independently predicts survival in patients with advanced cancer on treatment with immune checkpoint inhibitors.

Although immune checkpoint inhibitors (ICIs) are effective cancer drugs, ICI-induced diabetes is a rare but a life-threatening adverse event for patients. The deleterious action of ICI on pancreatic beta-cell function is a concern. However, the influence of ICI on insulin synthesis and secretion in patients with cancer without diabetes remains unknown. This study included 87 patients diagnosed with advanced cancer. Glucose metabolism markers (HbA1c, HOMA-IR) and indicators of insulin secretory capacity (HOMA-beta, C-peptide) were prospectively evaluated in patients with ICI-treated cancers to determine their association with cancer prognosis. Patients with overall survival (OS) ≥ 7 months had substantially higher HOMA-beta levels at baseline (p=0.008) and 1 month after ICI administration (p=0.006) compared to those with OS <7 months. The median OS was significantly longer in patients with HOMA-beta ≥ 64.24 (13 months, 95%CI: 5.849-20.151, 37 events) than in those with HOMA-beta < 64.24 (5 months, 95%CI: 3.280-6.720, 50 events) (p=0.013). Further, the median progression-free survival (PFS) was significantly longer in patients with HOMA-beta ≥ 66.43 (4 months, 95%CI: 3.073-4.927, 33 events) than in those with HOMA-beta < 66.43 (2 months, 95%CI: 1.410-2.590, 54 events) (p=0.025). Additionally, multivariable logistic regression analysis revealed that a HOMA-beta value ≥ 64.24 independently predicted longer OS in ICI-treated patients. Pre-ICI HOMA-beta level is linked to longer OS in ICI-treated patients. This connection is significant and shows that insulin secretory capacity may predict ICI efficacy.

Physical activity and cardiometabolic risk factors in sprint and jump-trained masters athletes, young athletes and non-physically active men

Abstract Objectives Assessing physical activity and cardiometabolic risk in masters athletes as an example of very high physical activity at old age. Methods Forty-three men were studied in full factorial design, either as sprint or jump-trained masters athletes (MA, n=10, age 60–75 years), as young sprint or jump-trained athletes (YA, n=10, age 20–35 years), older control participants (OC, n=11, age 60–75 years) or as young control participants (AC, n=12, age 20–35 years). We performed bio-electrical impedance analysis and assessed serum markers of lipids and glucose metabolism and C-reactive protein, structured training hours, and habitual activity via mobile actimetry. Results Body fat was greater in OC than in MA (23.9 [SD 4.2] % vs. 14.0 [SD 5.7] %, p&lt;0.001), and also greater than in YA and YC (both p&lt;0.001). Weekly training hours were comparable between MA and YA (7.9 [SD3.3] hours vs. 11.1 [SD 4.8] hours, p=0.69). Habitual walking distance was greater in MA than in OC (7,387 [SD 4,923] m/day vs. 4,110 [SD 1,772] m/day, p=0.039), and so was habitual running distance (667 [SD690] m/day vs. 132 [427] m/day, p&lt;0.001). HOMA-index was greater in OC than in MA (2.07 [SD 1.39] vs. 0.80 [SD 0.41], p=0.0039), and so was C-reactive protein (1.35 [SD 1.74] mg/l vs. 0.58 [SD 0.27] mg/ml, p=0.018), whereas serum lipids showed only moderate or no effect (all p between 0.036 and 0.07). Conclusions Improved body composition and physical activity levels in MA are associated with lower cardiometabolic risk, which seems more pronounced for insulin sensitivity and inflammaging than for lipid metabolism.

Expression markers of human skeletal muscle associated with disorders of glucose metabolism in the basal and postprandial state

BACKGROUND. Skeletal muscles play a key role in the organism’s carbohydrate metabolism. Dysregulation of insulin-dependent glucose uptake in skeletal muscle disrupts carbohydrate metabolism in the organism and can lead to the development of obesity and type 2 diabetes.AIM. To identify expression markers (genes) of human skeletal muscle associated with disorders of glucose metabolism in the basal state and after a mixed meal normalized for body mass.MATERIALS AND METHODS. The study involved three groups of 8 people: healthy volunteers, obese patients without and with type 2 diabetes. Venous blood samples were taken in the morning (09:00) after an overnight fast and 30 min, 60 min, 90 min, 120 min, and 180 min after ingestion of a mixed meal normalized by body mass (6 kcal/kg). Biopsy samples from m. vastus lateralis was taken before and 1 h after a meal to assess gene expression (RNA sequencing) and search for genes correlating with markers of impaired glucose metabolism in the basal and postprandial state.RESULTS. Strong correlations (|ρ|&gt;0.7 and p&lt;0.001) between the gene expression and the level of insulin, C-peptide, glucose or glycated hemoglobin in the basal and/or postprandial state was found for 75 genes. Of these, 17 genes had marked differences (&gt;1.5-fold) in expression between healthy people and patients, or differences in expression changes in response to a meal. We can note genes whose role in impaired glucose metabolism has already been shown earlier (FSTL1, SMOC1, GPCPD1), as well as a number of other genes that are promising for further study of the mechanisms of insulin resistance in skeletal muscle.CONCLUSION. Skeletal muscle expression markers were identified as promising candidates for future targeted studies aimed at studying the mechanisms of insulin resistance and searching for potential therapeutic targets.

Associations between blood markers of glucose metabolism and characteristics of circulating lymphocytes

AimsThe pathophysiology of diabetes is not fully understood; recent research indicates close relations with immunological alterations. Therefore, the aim of this study was to investigate the associations between markers of glucose metabolism and characteristics of blood lymphocytes in a population-based cohort. MethodsThe analysis was based on data from 219 non-diabetic participants of the MEGA study in Augsburg, Germany, who were recruited between 2018 and 2021. The majority of participants were examined two different times with a time lag of 9 months. Fasting venous blood samples were taken and oral glucose tolerance tests (OGTT) were performed at both visits. Immune cells were analyzed from fresh blood using flow cytometry. The associations between fasting blood glucose levels, glucose levels at 2 h after oral glucose bolus and glycated hemoglobin (HbA1c) concentrations and the quantity of different lymphocyte subsets were analyzed using linear mixed regression models with random intercept. P values were FDR-adjusted. ResultsHbA1c was negatively associated with the marginal zone B cells (IgD + CD27+ B cells). Fasting glucose was positively associated with natural killer (NK) cells and 2-h OGTT glucose was positively associated with NKT cells. Finally, HbA1c showed significantly negative associations with the CD57-PD1-NKT cell subset. ConclusionMarkers of glucose metabolism showed significant associations with B cell, NK cell and NKT cell subsets, which clearly indicates a relation between glucose metabolism and the adaptive immune system.

Interaction of CETP rs708272 Polymorphism on Trans Fatty Acid Intake and Glucose Metabolism Markers.

Dietary fats influence gene expression and several metabolic pathways. Therefore, it is crucial to study the role of personal genotypes in the interaction between fat consumption and cardiometabolic markers. This research aimed to determine the interaction of the rs708272 polymorphism of CETP and the fatty acid intake with changes in the HOMA-IR in adults living with overweight or obesity. The current study was a secondary analysis of an 8-week controlled clinical trial. The final sample for this analysis comprised 78 Mexican adults with the Cholesteryl Ester Transfer Protein (CETP) rs708272 polymorphism who followed a dietary intervention. Using an interaction analysis, we evaluated the fatty acid intake and the genotypes of rs708272, with changes in blood glucose, insulin, and the HOMA-IR from baseline to endpoint. Our findings suggest a significant interaction between the trans fatty acid intake and the GG genotype with changes in glucose (p = 0.024), insulin (p = 0.004), and the HOMA-IR (p = 0.002). The higher the consumption of trans fatty acids, the less these markers of glucose metabolism were reduced. carriers of the GG genotype may benefit from limiting dietary trans fatty acid intake, as there was no reduction in plasma glucose and insulin despite a hypocaloric dietary intervention in adults with overweight and obesity.

Semaglutide modulates adipogenic differentiation and extracellular acidification in epicardial (EAT) and subcutaneous (SAT) adipose tissue stromal cells from patients with cardiovascular disease

Abstract Backround Cardiovascular disease (CVD) is the main cause of death in the world. One of the known risk factors is the epicardial fat (EAT) accumulation, which is around the myocardium and coronaries playing a paracrine role over them. Although mature and functional adipocytes are involved in energy balance and glucose metabolism, the hypertrophic state increases the production of fatty acid binding protein 4 (FABP4), which is a pro-inflammatory adipokine, with consequences on extracellular acidification. Recent data shows that glucagon-like peptide receptor agonists 1 (GLP1ra) drug improves the insulin response and reduces EAT thickness. Although GLP1ra has a direct effect on hypothalamus for reducing food intake, this drug might play a direct role on adipogenesis process in this fat stromal cells. Purpose Our study aims to demonstrate the effect of semaglutide on adipogenesis and metabolism in epicardial and subcutaneous stromal cells from patients with cardiovascular disease. Methods The study was approved by the Galician Research Ethics Committee, and subcutaneous adipose tissue (SAT) and EAT samples from 17 patients were obtained undergoing open-heart surgery with informed consent. Stromal cells from biopsies were isolated and cultured. Adipogenesis was induced for 15 days with or without 1 nM semaglutide, given by Novo-Nordisk (Bagsværd, Denmark), using an adipogenesis cocktail. Cells were lysed and RNA was isolated for RT-qPCR. Target genes were amplified for Glucagon like peptide 1- receptor (GLP1R), differentiation, adipogenesis, glucose metabolism and cellular markers. Extracellular acidification rate was measured with glycolytic rate assay on Seahorse. Lipids accumulation was tested by AdipoRed staining. Results Stromal cells from both tissues express GLP1R but higher differentiation factor (PGC1α) was detected in SAT compared to EAT (p=0.02), as well as adipogenesis induction. After semaglutide treatment, we observed a downregulation of FABP4 and GLUT1 in EAT (p=0.01 and p=0.02, respectively). Despite FABP4 was not modulated on SAT, there was a reduction of PGC1α levels. (p=0.02). Since glitazones upregulate PGC1α, which is used for adipogenesis induction, these results might suggest the counteract mechanism of semaglutide. The metabolism assay showed that semaglutide reduces extracellular acidification rate in EAT cells (p=0.04) and oxidative glycolysis with semaglutide treatment (p=0.003) but not in SAT cells. Conclusions Semaglutide reduces adipogenesis, through modulation of PGC1α transcription factor in EAT from patients with cardiovascular disease and extracellular acidification and oxidative glycolysis. These results might help to understand one of the mechanisms associated with EAT reduction in patients with semaglutide treatment.

Effects of metformin and curcumin in women with polycystic ovary syndrome: A factorial clinical trial

BackgroundPolycystic ovary syndrome (PCOS) is a common endocrine disorder in women, associated with dyslipidemia, insulin resistance, and hormonal imbalances. Metformin and curcumin have shown promise in improving these metabolic and hormonal parameters individually, but their combined effects in PCOS remain unclear. MethodsWe conducted a randomized, double-blind, placebo-controlled, 12-week factorial trial involving 200 women with PCOS. Participants were randomly assigned in a 1:1:1:1 ratio to receive metformin (500-mg/8 h) + placebo, nanocurcumin soft gel capsule (80-mg/8 h) + placebo, metformin (500-mg/8 h) + nanocurcumin (80-mg/8 h), or double placebo. Lipid profiles, glucose metabolism markers, hormonal parameters, body weight, and body mass index (BMI) were assessed at baseline and week 12. ResultsThe combination of metformin and curcumin demonstrated significant improvements in lipid profiles, glucose metabolism, hormonal parameters, body weight, and BMI compared to individual agents or placebo. Greater reductions in low-density lipoproteins (LDL) cholesterol, total cholesterol (TC), and triglyceride (TG) levels were observed with the combination therapy, along with increased high-density lipoproteins (HDL) cholesterol. Additionally, the combination therapy significantly improved markers of glucose metabolism and showed synergistic effects in reducing body weight and BMI. Reductions in testosterone and improvements in Follicle-stimulating hormone (FSH) and Luteinizing hormone (LH) levels were also observed with combination therapy. ConclusionThe combination of metformin and curcumin demonstrates superior efficacy in improving lipid profiles, glucose metabolism, hormonal parameters, body weight, and BMI in women with PCOS compared to individual agents or placebo. This highlights the potential synergistic effects of combining these agents for the management of PCOS.

Associations of the cardiometabolic index with insulin resistance, prediabetes, and diabetes in U.S. adults: a cross-sectional study

BackgroundThe cardiometabolic index (CMI) is a novel metric for assessing cardiometabolic health and type 2 diabetes mellitus (DM), yet its relationship with insulin resistance (IR) and prediabetes (preDM) is not well-studied. There is also a gap in understanding the nonlinear associations between CMI and these conditions. Our study aimed to elucidate these associations.MethodsWe included 13,142 adults from the National Health and Nutrition Examination Survey (NHANES) 2007–2020. CMI was calculated by multiplying the triglyceride-to-high density lipoprotein cholesterol (TG/HDL-C) by waist-to-height ratio (WHtR). Using weighted multivariable linear and logistic regression explored the relationships of CMI with glucose metabolism markers, IR, preDM, and DM. Nonlinear associations were assessed using generalized additive models (GAM), smooth curve fittings, and two-piecewise logistic regression.ResultsMultivariate regression revealed positive correlations between CMI and glucose metabolic biomarkers, including FBG (β = 0.08, 95% CI: 0.06–0.10), HbA1c (β = 0.26, 95% CI: 0.22–0.31), FSI (β = 4.88, 95% CI: 4.23–5.54), and HOMA-IR (β = 1.85, 95% CI: 1.56–2.14). There were also significant correlations between CMI and increased risk of IR (OR = 3.51, 95% CI: 2.94–4.20), preDM (OR = 1.49, 95% CI: 1.29–1.71), and DM (OR = 2.22, 95% CI: 2.00-2.47). Inverse nonlinear L-shaped associations were found between CMI and IR, preDM, and DM, with saturation inflection points at 1.1, 1.45, and 1.6, respectively. Below these thresholds, increments in CMI significantly correlated with heightened risks of IR, preDM, and DM.ConclusionsCMI exhibited inverse L-shaped nonlinear relationships with IR, preDM, and DM, suggesting that reducing CMI to a certain level might significantly prevent these conditions.

The Relationship Between Age at Diabetes Onset and Clinical Outcomes in Newly Diagnosed Type 2 Diabetes: A Real-World Two-Center Study.

This study was developed with the goal of clarifying whether there is any relationship between type 2 diabetes mellitus (T2DM) age of onset and clinical outcomes for patients in National Metabolic Management Centers (MMC). From September 2017 - June 2022, 864 total T2DM patients were recruited in MMC and assigned to those with early-onset and late-onset diabetes (EOD and LOD) based on whether their age at disease onset was ≤ 40 or > 40 years. All patients received standardized management. Baseline and 1-year follow-up data from these two groups of patients were assessed. Associations between onset age and other factors were evaluated with a multivariate linear regression approach, adjusting for appropriate covariates. Outcomes in particular subgroups were also assessed in stratified analyses. Markers of dysregulated glucose metabolism and BMI values were significantly higher among EOD patients as compared to LOD patients. Subjects in both groups exhibited significant improvements in several disease-related parameters on 1-year follow-up after undergoing metabolic management. EOD patients exhibited significantly greater percentage reductions in HbA1c levels (-28.49 (-44.26, -6.45)% vs -13.70 (-30.15,-1.60)%, P =0.017) relative to LOD patients following adjustment for confounders. Significant differences were also detected between these groups when focused on subgroups of patients who were male, exhibited a BMI ≥ 25, an HbA1c ≥ 9, or had a follow-up frequency < 2. Data from a 1-year follow-up time point suggest that a standardized metabolic disease management model can promote effective metabolic control in newly diagnosed T2DM patients, particularly among individuals with EOD.

Swimming exercise regulates indices of skeletal muscle glucose metabolism and attenuates cardiac inflammatory cytokines activity via IL-6/TNF-α pathway in streptozotocin-induced diabetic rats

Diabetes mellitus (DM) manifests with impaired glucose metabolism that affects the musculoskeletal and cardiovascular systems. This study investigated the effects of swimming exercise on some indices of muscle glucose metabolism and cardiac inflammatory markers in diabetic rats induced with streptozotocin. Wistar rats of both sexes (150–200 g) were assigned into five groups of seven (7) rats. Group 1: Control (CON), Group 2: Diabetes only (DM), Group 3: Exercise only (EX), Group 4: Diabetes + Exercise (DM + EX), Group 5: Diabetes + Insulin (DM + IN). Type 1 DM was induced via intraperitoneal injection of streptozotocin (60 mg/kg). Insulin (6 IU/g) was administered (IP) to animals in group 5. Swimming exercise test was done for 27 days after which animals were euthanized. Blood samples were collected while hamstring muscles and heart were harvested and homogenized to assess biochemical parameters. The body weight, serum insulin level, muscle glucose metabolic indices (glycogen, Glut-4, CK-MB), and cardiac troponin-T were significantly (P < 0.05) decreased. In contrast, the random blood glucose, cardiac TNF-α, and IL-6 levels were increased (P < 0.05) in diabetic rats when compared with the control group. Swimming exercise regimen significantly (P < 0.05) reversed these anomalies by reducing blood glucose and cardiac inflammatory cytokines (TNF-α and IL-6) levels, improving serum insulin, muscle glycogen, and GLUT-4 expression in diabetic rats when compared to the DM group. The cardiac inflammatory cytokine levels in DM + EX were comparable to the DM + IN group. In conclusion, swimming exercise improves muscle glucose metabolism and protects the heart against cardiac inflammation in diabetic conditions.