Insulin Sensitivity In Group Research Articles

SHBG Levels Do Not Correlate with Insulin Levels in PCOS with Appropriate Fasting Insulin Sensitivity

Introduction: There are several phenotypes of polycystic ovarian syndrome (PCOS), and the different phenotypes may differ metabolically. Methods: In the present retrospective study, women with PCOS having normal fasting insulin sensitivity (n = 88) were compared with women with PCOS showing impaired insulin sensitivity (n = 46) using the HPCOS (Hungarian Polycystic ovarian syndrome) database. Results: The impaired insulin sensitivity group has significantly higher body mass index (BMI) and HOMA index than the normal fasting insulin sensitivity group (BMI (kg/m2): 22.0 vs. 28.1, p < 0.0001, HOMA index: 0.96 vs. 2.38, p < 0.0001). The sex hormone binding globulin (SHBG) level was significantly lower, and the free androgen index proved itself significantly higher in the impaired insulin sensitivity group (p < 0.05). Linear regression analysis showed a negative association of BMI with SHBG levels in both groups, while BMI had a positive correlation with insulin concentrations in both groups. However, the SHBG levels were negatively associated with insulin concentrations in the impaired insulin sensitivity group, but this inverse association could not be observed in the normal fasting insulin sensitivity group. Conclusions: The inverse linear correlation of SHBG with HOMA index and serum insulin level is not evident in all PCO syndrome phenotypes, thus SHBG has limited applicability for characterizing carbohydrate metabolism and serum insulin sensitivity.

What is the relationship between serum uric acid level and insulin resistance?: A case-control study

Diabetes, arises from either an absolute or relative insufficiency of insulin or insulin resistance of peripheral tissues. For assessing long-term blood glucose concentration and insulin resistance, the utilization of glycosylated hemoglobin (HbA1c) and the Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) is widespread. Insulin resistance can lead to hyperuricemia by reducing the kidney ability to excrete urate, thus increasing sodium reabsorption. The aim of this study was to investigate the possible relationship between serum uric acid levels and insulin resistance. This was a retrospective case-control study. A total of 2530 applications in 2-year time were included in the study. Patient, known hypertension status, fasting plasma glucose, insulin, uric acid, HDL, low-density lipoprotein (LDL), triglyceride/Tg, HbA1c laboratory values and Tg/HDL ratio were examined. A statistically significant difference existed in the median uric acid values between the insulin-resistant and insulin-sensitive groups (P < .001). Additionally, a weak positive statistical correlation was identified between uric acid and HOMA-IR values (R = 0.299; P < .001) and uric acid and Tg/HDL values (R = 0.357; P < .001). This study concludes that there is a positive correlation between serum uric acid levels and insulin resistance.

Impaired Gonadotropin-Lowering Effects of Metformin in Postmenopausal Women with Autoimmune Thyroiditis: A Pilot Study.

Metformin has been found to reduce elevated gonadotropin levels. Hashimoto's thyroiditis is the most common thyroid disorder in iodine-sufficient areas, and it often develops in postmenopausal women. The aim of this study was to investigate whether autoimmune thyroiditis determines the impact of metformin on gonadotrope secretory function. Two matched groups of postmenopausal women were studied: 35 with euthyroid Hashimoto's thyroiditis (group A) and 35 without thyroid disorders (group B). Throughout the study, all participants received oral metformin (2.55-3 g daily). Plasma glucose, insulin, gonadotropins, estradiol, progesterone, thyrotropin, free thyroid hormones, prolactin, adrenocorticotropic hormone, insulin-like growth factor-1, hsCRP, thyroid peroxidase, and thyroglobulin antibody titers were measured at the beginning of the study and six months later. At entry, both groups differed in thyroid peroxidase antibody titers, thyroglobulin antibody titers, and hsCRP levels. In group A, baseline antibody titers correlated positively with hsCRP and negatively with insulin sensitivity. Although metformin improved glucose homeostasis and reduced hsCRP levels in both study groups, these effects were more pronounced in group B than in group A. Only in group B did metformin decrease FSH levels and tend to reduce LH levels. Thyroid antibody titers and the levels of the remaining hormones did not change throughout the study. The impact of metformin on gonadotropin levels correlated with their baseline values and the degree of improvement in insulin sensitivity, as well as with the baseline and treatment-induced reduction in hsCRP. Moreover, the impact on gonadotropins and insulin sensitivity in group A depended on baseline antibody titers. The obtained results indicate that coexisting autoimmune thyroiditis impairs the gonadotropin-lowering effects of metformin in postmenopausal women.

Effect of insulin resistance on CAC scores in cancer survivors.

e24056 Background: Many cancer (ca) survivors exhibit signs of insulin resistance (IR), an important risk factor for the development of coronary artery disease (CAD). Paramount in survivorship care is prevention of cardiovascular disease. Coronary artery calcium (CAC) scans offer a risk assessment of cardiovascular (CV) disease before cardiac damage has occurred. We investigated how IR affects CAC scores in cancer survivors. We hypothesized that CAC scores differ significantly between insulin-sensitive- and -resistant cancer survivors. Methods: We enrolled 90 cancer survivors of a large community hospital from March 2021 to January 2022 into this pilot study. Patients were subdivided into three groups: insulin-sensitive (IS), insulin-resistant/prediabetic and insulin-resistant/diabetic. Patients were tested for fasting insulin, -glucose, HgbA1c and lipids. Patients without evidence for prediabetes or diabetes also underwent an oral glucose tolerance test (oGTT). All patients received a CAC scan. Results: 32 patients were IS, 29 patients were IR/prediabetic and 29 patients were IR/diabetic. 17 CAC scans in the IS group, 6 CAC scans in the IR/prediabetic group and 5 CAC scans in the IR/diabetic group showed an Agatston score of 0. The p-value between the three groups was statistically significant ( p=0.005) where as the IR/prediabetic- and the IR/diabetic group did not differ statistically from each other. The mean MESA 10-year CHD risk with CAC was 7.8. There was a highly significant difference between the 3 groups: the IS group had a mean of 5.3, the IR/prediabetic group had a mean of 7.3, and the IR/diabetic group had a mean of 11.0 ( p < 0.001). The two IR groups did not differ statistically (p=0.076). Conclusions: Our study showed that IR including prediabetes significantly increases the MESA 10-yr. CHD Risk with CAC in cancer survivors. Survivors with IR also have less frequent zero CAC scores than insulin-sensitive survivors. Survivors disproportionately exhibit insulin resistance, partly due to the association of certain types of cancer with IR. This trial highlights the importance of screening survivors for IR. Survivors diagnosed with IR should be screened for CAD more frequently than the general population. CAC scans are an inexpensive and efficient way of screening asymptomatic cancer survivors for CAD.

Analysis of mRNA-miRNA-lncRNA differential expression in prediabetes/type 2 diabetes mellitus patients as potential players in insulin resistance.

Type 2 diabetes mellitus (T2DM) is a major global health concern. It usually develops gradually and is frequently preceded by undetectable pre-diabetes mellitus (pre-DM) stage. The purpose of this study was to identify a novel set of seven candidate genes associated with the pathogenesis of insulin resistance (IR) and pre-DM, followed by their experimental validation in patients' serum samples. We used the bioinformatics tools and through a two-step process, we first identified and verified two mRNA candidate genes linked to insulin resistance molecular pathogenesis. Second, we identified a non-coding RNAs related to the selected mRNAs and implicated in the insulin resistance molecular pathways followed by pilot study for the RNA panel differential expression in 66 patients with T2DM, 49 individuals with prediabetes and 45 matched controls using real time PCR. The levels of expression of TMEM173 and CHUK mRNAs, hsa-miR (-611, -5192, and -1976) miRNAs gradually increased from the healthy control group to the prediabetic group, reaching their maximum levels in the T2DM group (p <10-3), whereas the levels of expression of RP4-605O3.4 and AC074117.2 lncRNAs declined gradually from the healthy control group to the prediabetic group, reaching their lowest levels in the T2DM group (p <10-3). TMEM173, CHUK mRNAs, hsa_miR (-611 & -1976) and RP4-605O3.4 lncRNA were useful in distinguishing insulin resistant from insulin sensitive groups. miR_611 together with RP4-605O3.4 exhibited significant difference in good versus poor glycemic control groups. The presented study provides an insight about this RNA based STING/NOD/IR associated panel that could be used for PreDM-T2DM diagnosis and also as a therapeutic target based on the differences of its expression level in the pre-DM and T2DM stages.

Triglyceride/high-density lipoprotein ratio as a predictor for insulin resistance in a sample of healthy Iraqi adults.

Insulin resistance (IR) is a common pathophysiological condition associated with many metabolic diseases, including obesity, prediabetes, type 2 diabetes mellitus (T2DM), and cardiovascular disease. The widely used homeostasis model assessment for IR (HOMA-IR) is usually used to estimate IR. However, this model cannot be used for screening IR due to several logistic difficulties, such as costs and insulin instability, which are essential for measurement. Thus, finding feasible alternatives is of paramount importance. This study aimed to evaluate the value of triglyceride/high-density lipoprotein-cholesterol (TG/HDL-c) ratio in predicting IR in healthy adult individuals. The study involved 83 euglycemic non-diabetic adults (≥45 years old). Lipid profile, fasting insulin, fasting blood sugar (FBS), and glycated hemoglobin were measured for all participants. The TG/HDL-c ratio was calculated by dividing TG by HDL. Insulin resistance was calculated using the HOMA-IR formula. The receiver operating characteristic (ROC) curve was used to evaluate the predictive value of the TG/HDL-c ratio. The prevalence of IR among healthy adult Iraqis was 28.92%. Subjects in the IR group showed a higher TG/HDL ratio than the insulin-sensitive group (3.69±0.68 versus 2.71±1.0) with a significant difference. The area under the curve (AUC) for this ratio was 0.849, 95% CI= 0.763-0.935, p<0.002. The sensitivity and specificity of the test were 83% and 81%, respectively, at a best cut-off value of 3.1 (TG/HDL ratio). The prevalence of IR among healthy adult Iraqis was 28.92%. Triglyceride/HDL-c ratio had a very good predictive value for IR.

Effect of insulin resistance on CAC scores in cancer survivors

BackgroundMany ca. survivors exhibit signs of IR, an important risk factor for the development of CAD. CAC scans offer a risk assessment of CV disease before cardiac damage has occurred. We investigated how IR affects CAC scores in cancer survivors.ObjectivesThe aim of this study was to show that CAC scores differ significantly between insulin-sensitive- and -resistant cancer survivors.MethodsWe enrolled 90 cancer survivors of a large community hospital from March 2021 to January 2022 into this pilot study. Patients were subdivided into three groups: insulin-sensitive (IS), insulin-resistant/prediabetic and insulin-resistant/diabetic. All patients received a CAC scan.Results70% of asymptomatic survivors overall and 81% of asymptomatic IR patients show CAD on CAC scans. 17 CAC scans in the IS group, 6 CAC scans in the IR/prediabetic group and 5 CAC scans in the IR/diabetic group showed an Agatston score of 0. The p-value between the three groups was statistically significant (p = 0.005) whereas the IR/prediabetic- and the IR/diabetic group did not differ statistically from each other. The mean MESA 10-year CHD risk with CAC was 7.8. There was a highly significant difference between the 3 groups (p < 0.001). The two IR groups did not differ statistically (p = 0.076).ConclusionsSurvivors with IR including prediabetes have less frequent zero CAC scores than insulin-sensitive survivors. Our study also showed that IR including prediabetes significantly increases the MESA 10-yr. CHD Risk with CAC in cancer survivors. This trial highlights the importance of screening survivors for IR and draws attention to the association of IR to CAC not only in diabetes but also in prediabetes. The high fraction of asymptomatic survivors with CAD is concerning and calls for further investigation. CAC scans are an inexpensive and efficient way of screening asymptomatic cancer survivors for CAD.

Equine insulin dysregulation causes tissue specific alterations of proinflammatory cytokines and acute phase proteins in a NF-kB independent manner

Similar to human diabetes, equine metabolic syndrome (EMS) causes insulin dysregulation leading to debilitating sequela including laminitis. The pathophysiological mechanisms underlying EMS and laminitis are not well known. Therefore, using an insulin-resistant equine model, we hypothesized that insulin dysregulation induces an increased expression of inflammatory proteins in a tissue specific manner. Two groups of horses (n = -5/group) were categorized as insulin-resistant (IR) or insulin-sensitive (IS), using a frequently sampled intra-venous glucose tolerance test. Biopsies from skeletal muscle, and visceral and subcutaneous adipose tissues were collected in both groups. Protein expression was quantified via Western blotting in order to investigate HSP90, α 2 macroglobulin (A2M), Fibrinogen α, β, γ isoforms as well as cytokines, including interleukin-1β (IL-1β) and interleukin-6 (IL-6), in muscle and adipose tissues. Protein expression of HSP90, A2M and IL1-β was significantly greater in visceral adipose tissue of IR horses compared to IS horses. Fibrinogen (α and γ) expression was only significantly increased in subcutaneous adipose tissue of IR group compared to IS group. In contrast, no statistically significant difference in protein expression of proinflammatory cytokines and acute phase proteins was reported in skeletal muscle of IR vs. IS horses. Relative protein expression of total and phospho-NFκB protein expression was not statistically significantly changed in adipose tissues of IR horses compared to IS horses. In conclusion, proinflammatory cytokines and acute phase proteins were upregulated in adipose tissue, but not in skeletal muscle, through an NF-kB independent pathway. Insights from this study could reveal novel biomarkers and potential therapeutic targets for EMS.

Utility of Diabetes Type-Specific Genetic Risk Scores for the Classification of Diabetes Type Among Multiethnic Youth.

Genetic risk scores (GRS) aid classification of diabetes type in White European adult populations. We aimed to assess the utility of GRS in the classification of diabetes type among racially/ethnically diverse youth in the U.S. We generated type 1 diabetes (T1D)- and type 2 diabetes (T2D)-specific GRS in 2,045 individuals from the SEARCH for Diabetes in Youth study. We assessed the distribution of genetic risk stratified by diabetes autoantibody positive or negative (DAA+/-) and insulin sensitivity (IS) or insulin resistance (IR) and self-reported race/ethnicity (White, Black, Hispanic, and other). T1D and T2D GRS were strong independent predictors of etiologic type. The T1D GRS was highest in the DAA+/IS group and lowest in the DAA-/IR group, with the inverse relationship observed with the T2D GRS. Discrimination was similar across all racial/ethnic groups but showed differences in score distribution. Clustering by combined genetic risk showed DAA+/IR and DAA-/IS individuals had a greater probability of T1D than T2D. In DAA- individuals, genetic probability of T1D identified individuals most likely to progress to absolute insulin deficiency. Diabetes type-specific GRS are consistent predictors of diabetes type across racial/ethnic groups in a U.S. youth cohort, but future work needs to account for differences in GRS distribution by ancestry. T1D and T2D GRS may have particular utility for classification of DAA- children.

Prognostic significance of insulin resistance in pulmonary hypertension.

AimsThe relationship between insulin resistance (IR) and glucose intolerance with pulmonary hypertension (PH) has been suggested in recent investigations. In the present study, we aimed to show the prevalence of IR and its correlation with haemodynamic variables as well as its prognostic significance in this group of patients.Methods and resultsAmong 100 new and returning patients with PH, scheduled for right heart catheterization (RHC), 59 non‐diabetic patients were enrolled. The homeostasis model assessment of insulin resistance (HOMA‐IR) was used to assess IR. The study population were followed up for a median (interquartile range) of 48 (23–48) months for all‐cause mortalities. Most of the study population [mean (standard deviation) age of 45.9 (17.3)] were classified as class I of PH classification (47.5%). Overall, 27% of our study population had IR considering the Iranian cut points of HOMA‐IR. The prevalence of IR in non‐diabetic, non‐metabolic syndrome patients with precapillary PH (PAH) was 34.2%, which was higher than the prevalence of IR in non‐diabetic, non‐metabolic syndrome Iranian population (24.1%). There was no difference between IR and insulin sensitive (IS) groups regarding demographic and clinical findings, 6 min walk test, and laboratory and haemodynamic data in univariable and multivariable analyses. The mortality rate in the follow‐up period was 44.1%. The survival of patient with IR was slightly lower than IS patients; however, IR was not an independent predictor of death.ConclusionsThe glucose metabolism is dysregulated in patients with PH, and IR may increase the risk of adverse events among these patients.

Insulin sensitivity variations in apparently healthy Arab male subjects: correlation with insulin and C peptide

IntroductionDecreased insulin sensitivity occurs early in type 2 diabetes (T2D). T2D is highly prevalent in the Middle East and North Africa regions. This study assessed the variations in insulin sensitivity...

Insulin resistance attenuates the impact of levothyroxine on thyroid autoimmunity and hypothalamic-pituitary-thyroid axis activity in women with autoimmune subclinical hypothyroidism.

Subjects with both subclinical hypothyroidism and autoimmune thyroiditis are frequently diagnosed with metabolic syndrome. The purpose of the current study was to investigate whether insulin sensitivity determines levothyroxine action on thyroid antibody titres and hypothalamic-pituitary-thyroid axis activity in young women with autoimmune subclinical hypothyroidism. The study population consisted of three age-, thyroid antibody- and thyrotropin-matched groups of women with autoimmune subclinical hypothyroidism: metformin-naive women with insulin resistance (group A, n=31), women receiving metformin treatment because of insulin resistance (group B, n=32), as well as metformin-naive women with normal insulin sensitivity (group C, n=35). Throughout the study, all subjects were treated with levothyroxine. Titres of thyroid peroxidase and thyroglobulin antibodies, as well as circulating levels of glucose, insulin, lipids, thyrotropin, free thyroid hormones, prolactin, high-sensitivity C-reactive protein (hsCRP) and 25-hydroxyvitamin D were determined at the beginning of the study and 6months later. Except for two individuals, all patients completed the study. At baseline, group A differed from groups B and C in circulating levels of glucose, HDL-cholesterol, triglycerides, hsCRP, 25-hydroxyvitamin D and the homeostatic model assessment 1 of insulin resistance (HOMA1-IR). Although levothyroxine reduced thyroid antibody titres, decreased thyrotropin levels and increased free thyroid hormone levels in all studied groups, the effect on antibody titres and thyrotropin levels was more pronounced in groups B and C than in group A. The impact of levothyroxine on thyroid antibody titres correlated with baseline and treatment-induced changes in HOMA1-IR, thyrotropin, hsCRP and 25-hydroxyvitamin D. The results of the current study suggest that the impact of exogenous levothyroxine on thyroid autoimmunity and hypothalamic-pituitary-thyroid axis activity is determined by insulin sensitivity.

Gut Microbiota of Chinese Obese Children and Adolescents With and Without Insulin Resistance.

ObjectiveThe intestinal flora of gut microbiota in obese Chinese children and adolescents with and without insulin resistance (IR) was analyzed, as well as associations between the gut microbiota and two serum cytokines related to glucose metabolism, adropin and angiopoietin-like 4 (ANGPTL4).MethodsClinical data, fecal bacterial composition, glucose-related hormones, and serum adipokines (adropin and ANGPTL4) were analyzed in 65 Chinese children with exogenous obesity. The composition of the gut microbiota was determined by 16S rRNA-based metagenomics and IR was calculated using the homeostasis model assessment (HOMA).ResultsThe 65 obese subjects were divided into two groups: insulin sensitive (IS) (n=40, 57.5% males) or IR (n=25, 60% males). Principal coordinates analysis revealed that the gut microbiota samples from the IS group clustered together and separated partly from the IR group (p=0.008). By Mann-Whitney U-test, at a phylum level, a reduction of Firmicutes and an increase of Bacteroidetes in the IR subjects was observed. LEfSe analysis revealed that IS subject, when compared to their IR counterparts, harbored members of the order Coriobacteriales, Turicibacterales, Pasteurellales and family Turicibacteraceae, that were significantly more abundant. In contrast, the IR subjects had members of family Peptococcaceae that were significantly more prevalent than the IS subjects (all p<0.05). Spearman’s correlation analysis revealed that serum ANGPTL4 was positively associated with genus Bacteroides, Butyricimonas, and Alistipes, and adropin was positively associated with genus Anaerostipes and Alistipes, and negatively associated with genus Blautia (all p<0.05).ConclusionIn obese children, the gut microbiome in IR subjects was significantly discordant from the IS subjects, and the abundance of some metabolism-related bacteria correlated with the serum concentrations of adropin and ANGPTL4. These observations infer that the gut microbiota may be involved in the regulation of glucose metabolism in obesity.

Age-specific microbiota in altering host inflammatory and metabolic signaling as well as metabolome based on the sex

Metabolism is sex-different, and the direct link between gut microbiota and aging-associated metabolic changes needs to be established in both sexes. Gene expression, metabolic and inflammatory signaling, gut microbiota profile, and metabolome were studied during aging and after fecal microbiota transplantation (FMT) in mice of both sexes. Our data revealed young female mice and aged male mice were the most insulin sensitive and resistant group, respectively. In addition, aging reduced sex difference in insulin sensitivity. Such age- and sex-dependent metabolic phenotypes were accompanied by shifted gut microbiota profile and altered abundance of bacterial genes that produce butyrate, propionate, and bile acids. After receiving feces from the aged males (AFMT), the most insulin-resistant group, recipients of both sexes had increased hepatic inflammation and serum endotoxin. However, AFMT only increased insulin resistance in female mice and abolished sex difference in insulin sensitivity. Additionally, such changes were accompanied by narrowed sex difference in metabolome. Metabolomics data revealed that age-associated insulin resistance in males was accompanied by increased sugar alcohols and dicarboxylic acids as well as reduced aromatic and branched-chain amino acids. Further, receiving feces from the young females (YFMT), the most insulin-sensitive group, reduced body weight and fasting blood glucose in male recipients and improved insulin sensitivity in females, leading to enhanced sex differences in insulin sensitivity and metabolome. Aging systemically affected inflammatory and metabolic signaling based on the sex. Gut microbiome is age and sex-specific, which affects inflammation and metabolism in a sex-dependent manner.

Serum Lipase / Amylase Activity Ratio for Screening Insulin Resistance

Early diagnosis of insulin resistance (IR) is important to prevent the development of type 2 diabetes mellitus (DM). Type 2 DM is mainly considered as an endocrine disorder however some recent studies show that exocrine functions of the pancreas are insufficient in type 2 DM. Our aim in this study to evaluate the relation of insulin resistance with pancreatic exocrine functions. Fasting glucose, insulin, amylase, lipase, HbA1c, and demographic information of subjects were taken from the laboratory information system. Children and the diabetic subjects were excluded. Included subjects were separated according to the insulin sensitivity status determined by homeostatic model assessment. There were 335 individuals in the insulin sensitive (IS) group, 275 in the moderate IR group, and 164 in the severe IR group. The average age is 45 (34-54). Serum lipase and amylase levels were used as an indicator of pancreatic exocrine functions. Serum amylase, lipase and serum lipase/amylase activity ratio were compared between groups. Serum amylase levels were 67.8, 63 and 65.3 U/L; serum lipase levels were 31, 31 and 25.5 U / L, serum lipase/amylase ratios were 47%, 50% and 38% in the IS, moderate IR and severe IR groups, respectively. There is a significant difference in serum amylase levels between insulin- sensitive (IS) and moderate IR groups (p=0.02) and in serum lipase levels between IS and severe IR, and between moderate IR and severe IR (p<0.001, p<0.001 respectively). When we use serum lipase/amylase activity ratio to compare groups with each other, there is a significant difference between IS and moderate IR, IS and severe IR, and moderate IR and severe IR (p= 0.015, p<0.001, p< 0.001 respectively). Our results show that the exocrine functions of the pancreas are affected in insulin resistance and serum lipase/amylase activity ratio can be used as a new parameter to define and screen insulin sensitivity status of the body

Circulating microRNAs in insulin resistant horses and ponies

Insulin resistance is a prevalent disorder among horses and is associated with abnormal adiposity, laminitis, equine metabolic syndrome, and pituitary pars intermedia dysfunction. The processes leading to equine insulin resistance and associated conditions remain subject for study. MicroRNAs (miRNAs) are involved in regulation of many biological processes and diseases. The current study aimed to investigate the circulating miRNA profile of insulin resistant horses and ponies. It was hypothesized that insulin resistant horses would have a different circulating miRNA profile compared to healthy ones. 12 Thoroughbred/ Thoroughbred-cross and 12 Welsh/Dartmoor non-pregnant mares were evaluated for insulin sensitivity using frequent sampling intravenous glucose tolerance test (FSIGTT). Serum samples were collected for miRNA profiling through RT-qPCR analysis. Horses and ponies were divided into insulin sensitive (IS) or insulin resistant (IR) groups and their miRNA profiles compared. Results demonstrated that 13 miRNAs were differently expressed between IR and IS horses, 15 between IR and IS ponies, 17 between horses and ponies, and 10 between IR and IS animals (horses and ponies combined) (p<0.05). Finally, 8 miRNAs were proposed as potential regulators of equine insulin resistance. miRNA profiling is a potential tool to evaluate insulin resistance and associated conditions.

Serum Adipocytokines Levels and Their Association with Insulin Sensitivity in Morbidly Obese Individuals Undergoing Bariatric Surgery.

BackgroundObese adipose tissue secretes a variety of adipocytokines that act as metabolic regulators with complex mechanisms. Our objective was to compare serum concentration of a panel of adipocytokines between obese and non-obese individuals and identify any distinct patterns correlating with insulin sensitivity in obesity.MethodsWe designed a cross-sectional study among obese (body mass index [BMI] ≥30 kg/m2, n=62) and non-obese (BMI <25 kg/m2, n=32) individuals to compare circulating levels of the adipokines, such as adiponectin and resistin in conjunction with the measurement of the levels of inflammatory cytokines including C-reactive protein (CRP), interleukin (IL)-6, IL-8, monocyte chemoattractant protein (MCP)-1, and tumor necrosis factor (TNF)-α using Luminex multiplex immunoassay with drop array technology. Correlations between circulating adipocytokine levels and those of multiple well-established markers of insulin resistance including homeostatic model assessment of insulin resistance (HOMA-IR), homeostatic model assessment of β-cell function (HOMA-β) and quantitative insulin sensitivity check index were also established.ResultsCRP, IL-8, MCP-1, and TNF-α levels were higher in obese than non-obese individuals; the CRP and IL-8 differences were statistically significant. CRP correlated significantly with markers of insulin resistance (fasting plasma insulin, HOMA-IR, and QUICKI), and adiponectin correlated with HOMA-β in obese individuals. We divided the group of obese individuals on the basis of HOMA-IR levels into insulin-resistant (IR; HOMA-IR ≥2.5) and insulin-sensitive (IS; HOMA-IR <2.5) groups; and 43 out of 62 participants were IR despite comparable BMIs. An overall proinflammatory profile was compared between IR and IS obese, though the values were higher in IR obese but the difference was not significant.ConclusionObesity is associated with a general inflammatory milieu and a crosstalk between adipocytokines and insulin resistance is complex as well as multifactorial.

Evaluation of lipid ratios and triglyceride-glucose index as risk markers of insulin resistance in Iranian polycystic ovary syndrome women

BackgroundInsulin resistance has a vital role in the pathophysiology of polycystic ovary syndrome (PCOS). Previous investigations have shown that some lipid ratios could be a simple clinical indicator of insulin resistance (IR) in some disorders and ethnicities. The present study was conducted to evaluate the correlation between triglyceride to HDL-cholesterol (TG/HDL-C), total cholesterol to HDL-cholesterol (TC/HDL-C), as well as fasting triglyceride-glucose (TyG) indices with IR (as measured by homeostasis model assessment of IR (HOMA-IR), quantitative insulin sensitivity check index (QUICKI) and fasting glucose to insulin ratio (FGIR)) among the Iranian women diagnosed with PCOS.MethodsIn the current study, a total of 305 women with PCOS were evaluated. TG/HDL-C, TC/HDL-C, and TyG indices were calculated. Fasting insulin level was measured using ELISA technique. IR was defined as a HOMA-IR value of ≥2.63, FG-IR value of < 8.25, and QUICKI value of < 0.33.ResultsThe insulin-resistant (IR) and insulin-sensitive (IS) groups, established by the HOMA-IR, FG-IR, and QUICKI values were different in terms of TG/HDL-C, TC/HDL-C, and TyG indices. These indices were associated with IR even after adjusting for age and BMI. ROC curve analyses showed that TyG, TG/HDL-C, and TC/HDL-C strongly predicted HOMA-IR with area under the curve (AUC) of 0.639, 0.619, and 0.623, respectively (P < 0.05). Further, TC/HDL-C was a good predictor of FG-IR with AUC of 0.614 (P = 0.04).ConclusionTyG, TG/HDL-C, and TC/HDL-C indices might be good indicators of IR among Iranian women diagnosed with PCOS.

Resistin is not a useful insulin resistance marker for non-obese patients.

Resistin, an adipokine produced in fat tissue, may be linked to insulin resistance (IR) and type 2 diabetes. Previous data are controversial and have focused mainly on obese patients. We aimed to evaluate whether resistin plays a role in the development of IR in normal-weight individuals. The study involved 77 normal-weight participants. We defined IR using different indexes and cut-off points. Resistin, fasting insulin, glucose, and lipids concentrations and anthropometric parameters were measured. Serum resistin concentration was not associated with IR. Resistin concentration was weakly related to age in all insulin-sensitive groups and low-density lipoprotein cholesterol concentration in all IR groups. Moreover, a weak negative correlation between high-density lipoprotein cholesterol and resistin concentrations was observed in the IR group categorised by the 1.69 cut-off of the homeostasis model assessment of IR. The data suggest that resistin is not a useful marker for the prediction of IR in normal-weight individuals.

Are insulin-resistance and oxidative stress cause or consequence of aging.

Insulin resistance is associated with oxidative stress leading to cardiovascular diseases. However, little research has been performed examining elderly individuals with or without insulin-resistance. We demonstrate that antioxidant defense systems alone is not able to abrogate insulin action in elderly individuals at high risk for atherosclerosis, whereas the combined oxidant-antioxidant markers (thiobarbituric acid-reacting substances (TBARS), Cu,Zn-superoxide dismutase (SOD-1), and total antioxidant status (TAS)) might be more efficient and perhaps produce better clinical outcome. In fact, a decrease in oxidative stress and strong interaction between antioxidant defense can be seen only among insulin-resistant elderly individuals. This is, in our opinion, valuable information for clinicians, since insulin-resistance is considered strong cardiovascular risk factor.