Insulin Resistance In Obese Patients Research Articles

Context-dependent regulation of lipid accumulation in adipocytes by a HIF1α-PPARγ feedback network

Hypoxia-induced upregulation of HIF1α triggers adipose tissue dysfunction and insulin resistance in obese patients. HIF1α closely interacts with PPARγ, the master regulator of adipocyte differentiation and lipid accumulation, but there are conflicting results regarding how this interaction controls the excessive lipid accumulation that drives adipocyte dysfunction. To directly address these conflicts, we established a differentiation system that recapitulated prior seemingly opposing observations made across different experimental settings. Using single-cell imaging and coarse-grained mathematical modeling, we show how HIF1α can both promote and repress lipid accumulation during adipogenesis. Our model predicted and our experiments confirmed that the opposing roles of HIF1α are isolated from each other by the positive-feedback-mediated upregulation of PPARγ that drives adipocyte differentiation. Finally, we identify three factors: strength of the differentiation cue, timing of hypoxic perturbation, and strength of HIF1α expression changes that, when considered together, provide an explanation for many of the previous conflicting reports.

Anthropometric Indices With Insulin Resistance in Obese Patients: A Literature Review.

The hormone insulin is responsible for regulating the metabolism of proteins, carbs, and lipids by promoting the absorption of molecules such as glucose from the bloodstream into fat, the liver, and skeletal muscle cells. Insulin resistance (IR) is considered to be a physiological response to obesity that inhibits fat from accumulating and supports weight stabilization. People with IR gain less weight than those with insulin sensitivity, and therefore IR individuals have a three-fold increased likelihood of losing more weight when compared with insulin-sensitive individuals. A person's health is jeopardized by obesity, which is defined as excessive or unusual storage of fat in adipose tissue. Early identification using different anthropometric measuring parameters and proper and suitable therapy is essential as the incidence of obesity cases is increasing as a result of sedentary lifestyles, bad eating habits, a lack of physical exercise, and alack of knowledge among young adults. The review followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, following which based on inclusion and exclusion criteria, eight articles were considered for the review. The analysis showed that all the parameters are easily accessible and hence can be used in daily practices. Due to being readily available, body mass index (BMI) and waist circumference (WC) constituted the most often employed anthropometric measures in everyday practices. In addition, variances in the values of the variables were seen due to differences in gender.

PINK1 and oxidative stress in lean and obese patients with type 2 diabetes mellitus

AimTo compare mRNA [messenger RNA] expression of PINK1 in whole blood and the levels of biomarkers of Oxidative Stress (mitochondrial DNA [mtDNA] content & Total Antioxidant status [TAS]) in newly diagnosed lean and obese patients with T2DM. MethodsNewly diagnosed patients of T2DM were enrolled in this study. The patients were divided into two groups of 30 patients each, lean (BMI < 18.5 kg/m2) and obese (BMI > 25 kg/m2). mRNA expression of PINK1 & mtDNA content was measured by real time PCR. Serum TAS was measured using a commercially available kit. ResultsThere was a 1.78-fold decrease in mRNA expression of PINK1 in obese group compared to the lean group. Mean mtDNA content was 300.82 ± 169.66 in the obese group and 332.78 ± 147.07 in the lean group (p = 0.06). Mean levels of TAS was 5.39 ± 2.28 μM Trolox Equivalents in the obese group and 3.85 ± 3.33 μM Trolox Equivalents in the lean group (p = 0.001). ConclusionThe T2DM patient with obesity had greater OS than the lean patients. Thus, there is a compensatory increase in antioxidants in obese patients with T2DM. Our findings also suggest that decreased levels of PINK1 in obese group are unable to protect the mitochondria against OS leading to decreased mtDNA content. Does it also result in beta cell dysfunction or contribute to insulin resistance in obese patients with T2DM needs to be explored.

Relationship between serum Nesfatin-1, Adiponectin, Resistin Concentration, and Obesity with Type 2 Diabetes Mellitus

Diabetes mellitus caused by insulin resistance is prompted by obesity. Neuropeptide Nesfatin-1 was identified in several organs, including the central nervous system and pancreatic islet cells. Nesfatin-1 peptide appears to be involved in hypothalamic circuits that energy homeostasis and control food intake. Adiponectin is a plasma collagen-like protein produced by adipocytes that have been linked to the development of insulin resistance (IR), diabetes mellitus type 2 (DMT2), and cardiovascular disease (CVD). Resistin was first identified as an adipose tissue–specific hormone that was linked to obesity and diabetes. The aim of this study was to estimate the relationship between human serum nesfatin-1, adiponectin, resistin concentration, and obesity with T2DM. The results show a significant increase in serum neisfatin-1 and resistin levels in the obese diabetic group compared to the non-obese diabetic group. Adiponectin levels had a highly significant decrease in the obese diabetic group compared to the non-obese group and obese control group. Serum Nesfatin-1 and some variables, there was a significant positive correlation with (BMI, insulin, HOMA-IR), and serum resistin had a significant positive correlation with (BMI, WC, TG, insulin, HOMA-IR).On the other hand, there was a negative correlation between serum adiponectin and (BMI, TG, and HOMA-IR). The present results suggest that nesftin-1 may have a role in controlling food intake as well as the development of IR in obese patients.

High tissue-sodium associates with systemic inflammation and insulin resistance in obese individuals

Background and aimsHigh sodium intake is associated with obesity and insulin resistance, and high extracellular sodium content may induce systemic inflammation, leading to cardiovascular disease. In this study, we aim to investigate whether high tissue sodium accumulation relates with obesity-related insulin resistance and whether the pro-inflammatory effects of excess tissue sodium accumulation may contribute to such association. Methods and resultsIn a cross-sectional study of 30 obese and 53 non-obese subjects, we measured insulin sensitivity determined as glucose disposal rate (GDR) using hyperinsulinemic euglycemic clamp, and tissue sodium content using 23Na magnetic resonance imaging. Median age was 48 years, 68% were female and 41% were African American. Median (interquartile range) BMI was 33 (31.5, 36.3) and 25 (23.5, 27.2) kg/m2 in the obese and non-obese individuals, respectively. In obese individuals, insulin sensitivity negatively correlated with muscle (r = −0.45, p = 0.01) and skin sodium (r = −0.46, p = 0.01). In interaction analysis among obese individuals, tissue sodium had a greater effect on insulin sensitivity at higher levels of high-sensitivity C-reactive protein (p-interaction = 0.03 and 0.01 for muscle and skin Na+, respectively) and interleukin-6 (p-interaction = 0.024 and 0.003 for muscle and skin Na+, respectively). In interaction analysis of the entire cohort, the association between muscle sodium and insulin sensitivity was stronger with increasing levels of serum leptin (p-interaction = 0.01). ConclusionsHigher muscle and skin sodium are associated with insulin resistance in obese patients. Whether high tissue sodium accumulation has a mechanistic role in the development of obesity-related insulin resistance through systemic inflammation and leptin dysregulation remains to be examined in future studies.Clinicaltrials.gov registration: NCT02236520.

The relationship between physical activity and diabetes in middle-aged and elderly people.

To investigate the association between diabetes symptoms and physical activity (PA) levels among middle-aged and older Chinese adults. Data for this study were obtained from 2018 Charles data. Z test, logistic regression analysis, and linear hierarchical regression analysis were performed in 5352 individuals aged ≥50 years with complete information. In terms of diabetes, 6.8% of the middle-aged and elderly people with diabetes were detected, and 93.2% of the middle-aged and elderly people without diabetes symptoms. The proportion of middle-aged and elderly people with high PA levels was 50.5%, and the proportion of middle-aged and elderly people with low PA was 49.5%. There was a significant positive correlation between low PA and diabetes (P < .05). After adjusting demographic characteristics (gender, registered permanent residence type, education level, age, widowhood) and health status characteristics (poor mood, asthma, hyperlipidemia, disability, memory disease, self-assessment of health status, hypertension, smoking, stroke, depression), there was still a statistical significance between PA level and diabetes (P < .05). The risk of diabetes of middle-aged and elderly people in China increases with age, while the risk of diabetes of middle-aged and elderly people with low level of PA is higher. The risk of diabetes is high among middle-aged and elderly people who are old, have poor self-evaluation health, suffer from hyperlipidemia, memory disease, and asthma. The middle-aged and old people should increase their PA levels to prevent and improve diabetes.

Düşük serum meteorin benzeri/subfatin seviyesi, obezite ve insülin direnci ile ilişkilidir

Introduction: Meteorin-like (Metrnl), also known as subfatin is a newly discovered adipokine of adipocyte origin that may play a role in obesity and insulin resistance. The current study aimed to investigate the association between subfatin and biochemical values, demographic characteristics, and insulin resistance in obese patients and healthy controls.Methods: This cross-sectional study included 59 obese patients with sex and age-matched group of 41 healthy controls. An enzyme-linked immunosorbent assay (ELISA) was used to measure the serum levels of Subfatin (Metrnl), and the correlations of Metrnl level with anthropometric parameters, HOMA index, and biochemical measurements were assessed.Results: The levels of BMI (p&amp;lt;0.001), insulin (p=0.002), and HOMA-IR score (p&amp;lt;0.001) were significantly higher in obese patients than controls. The serum levels of Subfatin were found to be lower in obese patients (1.85 [1.35–5.51] ng/ml) compared to the healthy controls (21.82 [12.61–27.76] ng/ml) (p&amp;lt;0.001). Subfatin had a significantly negative relationship with age (r =-0.250, p=0.012), weight (r =-0.373, p=0.001), BMI (r =-0.492, p=0.001), HbA1c (r =-0.209, p=0.037), LDL (r =-0.264, p=0.008), HOMA-IR (r =-0.223, p=0.026), and glucose (r =-0.376, p&amp;lt;0.001). There was a significantly positive correlation between subfatin and height (r=0.321, p=0.001).Conclusion: These results show that levels of subfatin were decreased in obese patients. There is a relationship between circulating amounts of subfatin hormone and age, weight, height, LDL-cholesterol, glucose, hbA1c, and HOMA-IR. Subfatin might be a new biomarker of obesity and insulin resistance.Keywords: Meteorin-like/subfatin, adiposity, insulin resistance, adipokines, biomarkers, diabetes mellitus type 2

Homeostatic microbiome disruption as a cause of insulin secretion disorders. Candida albicans, a new factor in pathogenesis of diabetes: A STROBE compliant cross-sectional study.

The study aimed to test the hypothesis that homeostatic microbiome (HM) disorders lead to the increased indirect influence of certain microorganisms (MO) in the gastrointestinal tract, causing a disorder of insulin secretion, insulin resistance, and diabetes. We highlighted Candida and certain types of bacteria since previous in vitro research showed they significantly affect insulin secretion and can cause insulin resistance in obese patients with metabolic syndrome. After determining the type of MO present in the throat swab and the stool, the oral glucose tolerance test (OGTT) test, and analysis of glucose and insulin secretion were performed in patients (n = 38) who were positive for certain types of MO compared to negative patients. Finally, all patients were divided into two groups: overweight patients (body mass index [BMI] < 30) and obese patients (BMI > 30). These two groups were compared for the percentage of certain types of MO to determine which MO can affect an increase in obesity and BMI. The presence of Diphtheroids in the throat (60.5%) reduces insulin secretion in patients compared with the negative group (194.5: 332.4) and the difference was statistically significant (P = .030). The presence of Candida in the throat (10%) increases insulin secretion, but the difference was statistically insignificant. The presence of Candida in the stool (28.9%) also increases insulin secretion and the difference was statistically significant (P = .038). Cumulative results (throat + stool) were similar (180: 332, P = .022). Analysis of BMI showed that the percentage of Diphtheroids in the throat decreases with increased body weight (53.8: 75%) while the percentage of Candida (38.5: 8.3%) and Enterobacter (61.5: 25%) increases, but these differences were statistically insignificant (P > .05). Diphtheroids in the throat can reduce insulin secretion by synthesizing their metabolites. Candida albicans is a conditional pathogen and as a significant indirect factor induces increased insulin secretion and insulin resistance. There are indications that elevated levels of Candida in the intestinal system can cause increased body weight of patients. C albicans should be considered a new factor in the pathogenesis of diabetes.

RF36 | PMON301 The Local Androgen-Estrogen Environment Differentially Regulates Adipocyte Lipid Metabolism by Fat Depot and Sex

Abstract Obese men often have low blood testosterone (Test) levels yet may have high or low blood 17β-estradiol (E2) levels while showing an increased risk of type 2 diabetes. In contrast, women with polycystic ovary syndrome (PCOS) experience increased risk of visceral white adipose tissue (vWAT) deposition, insulin resistance, and cardiovascular disease. Overall, insulin resistance is correlated with hypoandrogenemia in males and hyperandrogenemia in females. The aim of the present study was to elucidate the sexually dimorphic role androgens play in regulating the adipocyte insulin signaling pathway. We hypothesized that androgens would upregulate insulin signaling pathway components in female vWAT adipocytes irrespective of E2 levels. We further hypothesized that androgens would downregulate insulin signaling pathway components in male vWAT adipocytes dependent on E2 levels. vWAT and subcutaneous white adipose tissue (scWAT) were collected from male and female rats, digested in sterile-filtered collagenase, and the resulting preadipocytes were proliferated to 80% confluence. After cell cultures were induced to a minimum of 60% adipocyte cells, cells were exposed to the following treatments: no steroid, 5a-dihydrotestosterone (DHT), E2, Test, fulvestrant, Test + letrozole, and Test + fulvestrant for 48 hours. Adipocyte protein was western blotted for Total AKT and p-AKTSer473 and normalized to GAPDH. qPCR was performed to quantify insulin receptor (Insr), insulin receptor substrate 1 (Irs1), protein kinase B isoform 2 (Akt2), fork head box protein 1 (Foxo1) using the housekeeping gene Gapdh. 48-hour steroid treatments of E2 reduced pAKTSer473: AKT compared with that of controls in male vWAT. Interestingly, pAKTSer473: AKT of E2-treated male scWAT was unchanged compared with control levels. Yet, for both male scWAT and vWAT, Test and fulvestrant treatments had greater pAKTSer473: AKT than in E2-treated cells, while T + letrozole-treated male scWAT also showed higher pAKTSer473: AKT than in E2 treatments. In contrast, T + fulvestrant increased pAKTSer473: AKT in female vWAT. Protein data for females and Foxo1 protein are still being generated. At the RNA level female scWAT had upregulated Insr in response to Test + fulvestrant and Akt2 and Foxo1 to Test+ fulvestrant. In both male and female vWAT fulvestrant upregulates the Insr. As we see differences in the Test, fulvestrant and letrozole treatments, the control of local androgens over insulin signaling in WAT may vary by local ERa and ERβ expression and/or steroidogenesis. Furthermore, estrogenic effects on insulin signaling seem to vary by fat depot in males. Thus, sex-specific pharmaceuticals targeting the intersection of androgens, estrogens, and AKT in WAT can be an important tool in the treatment of insulin resistance in obese patients. Presentation: Monday, June 13, 2022 12:30 p.m. - 12:35 p.m., Monday, June 13, 2022 12:30 p.m. - 2:30 p.m.

Association between adipokines and cardiac remodeling in obese patients in preclinical heart failure

Introduction. Association of left ventricular hypertrophy (LVH) in obesity and accompanying metabolic risks with adipokines levels at the different stage of heart failure (HF) is still debatable.The aim of study was to investigate the relationship of circulating adipokines levels with LVH in obese patients at preclinical stage of HF.Materials and methods. The study included 74 obese patients: 43% had no markers of LVH (stage A HF, group 1); 57% had LVH (stage B HF, group 2). Transthoracic echocardiography, laboratory assessment of N-terminal fragment of the brain natriuretic peptide, soluble suppression of tumorigenesis-2 (sST2), circulating leptin and adiponectin levels, homeostasis model assessment of insulin resistance (IR) (HOMA-IR) were done. Matched-pairs analysis was applied.Results. Negative correlations of LVH with leptin levels in group 1 (stage A HF) and with adiponectin levels in group 2 (stage B HF) were detected (all p &lt; 0.05). Positive correlations of the sST2 / adiponectin ratio and HOMA-IR with the parameters of LVH were detected in group 2 (all p &gt;&lt; 0.05). Conclusion. The direction of the associations between circulating adipokines and LVH varies with the preclinical stage of HF. The data obtained may reflect a relationship between heart remodeling in response to molecular mechanisms of inflammation and IR in obese patients at the certain stage of cardiovascular continuum. Keywords: leptin, adiponectin, insulin resistance, HOMA-IR, inflammation, sST2, left ventricular hypertrophy&gt;˂ 0.05). Positive correlations of the sST2 / adiponectin ratio and HOMA-IR with the parameters of LVH were detected in group 2 (all p ˂ 0.05).Conclusion. The direction of the associations between circulating adipokines and LVH varies with the preclinical stage of HF. The data obtained may reflect a relationship between heart remodeling in response to molecular mechanisms of inflammation and IR in obese patients at the certain stage of cardiovascular continuum.

Relationship between insulin-biochemical resistance levels and the degree of depression and anxiety in patients from Honduras

Background/purposeMany studies suggest that insulin resistance in obese patients bridges mental illness. Our objective was to identify the association between levels of depression and anxiety with insulin resistance, and its relationship with obesity and abdominal obesityMethodsA cross-sectional analytical study was carried out in Honduras. Sociodemographic variables, anthropometric parameters, HOMA index, and level of severity of anxiety and depression were collected, and a descriptive, bivariate, and multivariate were performed.ResultsIn a sample of 381 adult patients, the bivariate analysis showed a statistic association of insulin resistance with all remaining variables. However, multivariate analysis showed a significative association of anxiety with BMI, depression, waist circumference, and insulinemia, while depression was associated with HOMA, anxiety, insulinemia, glycemia, and waist circumference.ConclusionsOur results provide important evidence of a direct and growing association between HOMA-IR and the severity of depression, and indirectly with anxiety. Secondarily, also with anthropometric factors (BMI and WC), traditionally associated with cardiovascular risk. This finding has important implications both for the early diagnosis of these mental pathologies, taking into account HOMA-IR values, and for preventive interventions focused on maintaining blood insulin levels.

A study of the effect of yoga on C-reactive protein, lipid profile and insulin resistance in obese patients

Background: Obesity is defined as a state of excess adipose tissue mass. In the last decade, there has been an alarming prevalence of obesity in the developed and developing countries like India. While modern medicine has so far been unable to control the menace of obesity, yoga offers an alternative holistic approach to tackle the problem of obesity by inculcating an approach towards balanced diet (Satwik aahar), physical activity and behavior modification (through pranayama). In this study, we have included the core anthropometric parameters of obesity, as well as associated abnormalities secondary to obesity like, insulin resistance, glucose intolerance, hypertension, atherogenic dyslipidemia.Methods: The study was conducted in the department of medicine, L. L. R. M. Medical College and associated S. V. B. P. Hospital, Meerut, U.P. during 2020-2021 with the objective to assess the role of yoga therapy in modifying anthropometric and biochemical parameters of obese patients. It was a prospective, controlled trial in which 120 obese patients (BMI≥25 kg/m2) were enrolled and followed for a period of six months.Results: Yoga therapy along with dietary restrictions is highly effective in improving the various anthropometric and biochemical parameters in obese patients and also beneficial in controlling complications like hypertension, diabetes and dyslipidemias secondary to obesity. It also improved the quality of life of these patients.Conclusions: This study is a modest attempt to ascertain the role of yoga in obesity and it hopes to encourage further research in the field.

Microbiota and adipocyte mitochondrial damage in type 2 diabetes are linked by Mmp12+ macrophages.

Microbiota contribute to the induction of type 2 diabetes by high-fat/high-sugar (HFHS) diet, but which organs/pathways are impacted by microbiota remain unknown. Using multiorgan network and transkingdom analyses, we found that microbiota-dependent impairment of OXPHOS/mitochondria in white adipose tissue (WAT) plays a primary role in regulating systemic glucose metabolism. The follow-up analysis established that Mmp12+ macrophages link microbiota-dependent inflammation and OXPHOS damage in WAT. Moreover, the molecular signature of Mmp12+ macrophages in WAT was associated with insulin resistance in obese patients. Next, we tested the functional effects of MMP12 and found that Mmp12 genetic deficiency or MMP12 inhibition improved glucose metabolism in conventional, but not in germ-free mice. MMP12 treatment induced insulin resistance in adipocytes. TLR2-ligands present in Oscillibacter valericigenes bacteria, which are expanded by HFHS, induce Mmp12 in WAT macrophages in a MYD88-ATF3-dependent manner. Thus, HFHS induces Mmp12+ macrophages and MMP12, representing a microbiota-dependent bridge between inflammation and mitochondrial damage in WAT and causing insulin resistance.

MOLECULAR BASIS OF THE DEVELOPMENT OF INSULIN RESISTANCE IN OBESE ADOLESCENT AND ADULT MEN

The aim of this work was to study the association between the expression of glucose metabolism related genes and insulin resistance, which expression is changed in obese adolescents and adult men with and without insulin resistance, for better understanding the molecular basis of the development of obesity complications and evaluation of possible contribution of these genes in development of insulin resistance. Methods. The expression level of genes related to glucose metabolism and their regulations was studied by real-time qPCR in adipose tissue and blood cells using SYBRGreen Mix and specific for each mRNA forward and reverse primers. Total RNA was extracted using TRIZOL reagent. For reverse transcription of mRNAs we used Thermo Scientific Verso cDNA Synthesis Kit (Germany). The values of mRNA expressions were normalized to the level of ACTB mRNA and represented as percent of control (100 %). Results. It was shown that in obese patients with insulin resistance the expression level of IRS1 (insulin receptor substrate 1), HK2 (hexokinase 2), PFKFB2 (6-phosphofructokinase/fructose-2,6-bisphosphatase 2) and PFKFB3 as well as circadian factors CLOCK and ARNTL genes in subcutaneous adipose tissue is significantly decreased as compared to obese men with normal sensitivity to insulin. At the same time, the development of insulin resistance in obese patients leads to up-regulation of PFKFB4, PER1, HSPA6, ALDH1A3, COL5A1, TIMP1, TIMP2, SPARC, and VCAN gene expressions in subcutaneous adipose tissue. The expression level of IGF1 (insulin-like growth factor 1) and IGFBP5 (IGF binding protein 5) as well as ENO1 (enolase 1) and ENO2 is down-regulated in the blood of obese adolescent with insulin resistance, but IGFBP2 and IGFBP7 gene expressions are significantly increased in these patients. Conclusions. The results of this investigation provide evidence that the development of insulin resistance in obese patients is associated with gene specific changes in the expression of many very important regulatory genes, which are endoplasmic reticulum stress responsible.

Fibroblast Growth Factor 21 as a Marker of Prediabetes in Patients with Non-alcoholic Fatty Liver Disease.

Fibroblast growth factor 21 is a peptide primarily secreted by the liver in response to peroxisome proliferator-activated receptor-α activation which plays an important role in regulating carbohydrate and lipid metabolism. This study investigated the association between fibroblast growth factor 21 and prediabetes in obese patients with non-alcoholic fatty liver disease in adult population. A total of 85 obese non-alcoholic fatty liver disease patients without (n = 49) and with prediabetes (n = 36) were included. Serum fibroblast growth factor 21 levels were determined by enzyme-linked immunosorbent assay. Higher fibroblast growth factor 21 serum levels were observed in patients with prediabetes, metabolic syndrome, dyslipidemia, and insulin resistance. There were significant correlations between fibroblast growth factor 21 and waist-to-stature ratio, visceral adiposity index, triglycerides, very low-density lipoproteins, alanine aminotransferase (ALT), gamma-glutamyl transferase (GGT), Quantitative Insulin Sensitivity Check Index, and Stumvoll index of insulin sensitivity. Fibroblast growth factor 21 level ≥320 pg/mL was associated with a 4.2-fold higher risk of prediabetes and ≥270 pg/mL for metabolic syndrome approximately 4 times. Fibroblast growth factor 21 is associated with increased risk for prediabetes, metabolic syndrome, and insulin resistance in obese patients with non-alcoholic fatty liver disease.

Marine Oil from C. finmarchicus Enhances Glucose Homeostasis and Liver Insulin Resistance in Obese Prediabetic Individuals.

The intermediate state between normal glucose tolerance and overt type 2 diabetes mellitus is associated with micro- and macrovascular diseases, requiring safe and cost-effective treatment measures interventions. A novel source of LC n-3 FAs is Calanus finmarchicus Oil, which showed promising effects on glucose homeostasis in preclinical studies due to anti-obesity effects and/or anti-inflammatory properties. In total, 43 obese patients (BMI: 31.7 ± 5.2 kg/m2) were allocated in the following two groups: (1) Calanus oil group (2 g CO/day) and (2) placebo group (2 g paraffin oil/day). Markers of glucose metabolism, body composition and energy intake were measured at the beginning (t0), after 12 weeks (t12) and 16 weeks (t16). Overall, parameters reflecting abnormal glucose homeostasis and insulin resistance in the liver, including fasting insulin (−2.9 mU/L ± 4.10, p < 0.05), HOMA-IR (−0.9 ± 1.28, p < 0.05) and hepatic insulin resistance index (−1.06 ± 1.72 × 106, p < 0.05) significantly enhanced after a 12-week CO-intervention, while no differences were observed in HbA1c, AUC0–2h Glucose, AUC0–2h Insulin, 2 h plasma glucose and muscle insulin sensitivity index. Our results indicate that Calanus oil causes beneficial effects on glucose metabolism and insulin resistance in obese patients, with clinical relevance to be verified in further studies. In addition, the possible active compounds and their mechanisms of action should be elucidated.

Macrophage activation marker sCD163 is associated with liver injury and hepatic insulin resistance in obese patients before and after Roux-en-Y gastric bypass.

BackgroundMacrophages are associated with metabolic complications to obesity including fatty liver disease and impaired hepatic and muscle insulin sensitivity (IS). Bariatric surgery induces weight loss and improves IS. We investigated associations between the macrophage activation marker soluble (s)CD163, alanine‐aminotransferase (ALT), and IS before and after Roux‐en‐Y Gastric Bypass (RYGB).MethodsWe analyzed sCD163 from 10 type 2 diabetes (T2D) and 10 obese patients with normal glucose tolerance (NGT) undergoing RYGB for associations with hepatic, adipose tissue, and muscle IS and ALT after 1‐week, 3, and 12 months postoperatively. IS was evaluated by hyperinsulinemic‐euglycemic clamp in combination with glucose tracer technique.ResultsPreoperative sCD163 correlated with ALT (r = 0.58, p = 0.007) and tended to associate inversely with hepatic (r = −0.39, p = 0.1) and adipose tissue (r = −0.39, p = 0.09), but not muscle IS. Following RYGB, sCD163 decreased significantly in all patients. The decrease in sCD163 during the first 3 months correlated inversely with the improvement of hepatic IS (r = −0.65, p = 0.01) and tended to be associated with changes in muscle IS (r = −0.45, p = 0.09). After 3 months sCD163 remained associated with ALT (r = 0.75, p < 0.001) and inversely with hepatic IS (r = −0.39, p = 0.1), but not muscle or adipose tissue IS. One year after RYGB, sCD163 correlated with ALT (r = 0.61, p = 0.007), but not with hepatic, adipose tissue, or muscle IS.ConclusionMacrophage activation is associated with liver injury and hepatic IS in obese patients. Improvements in these measures correlate during the first 3 months following RYGB, supporting a link between macrophages and hepatic IS in severe obesity and diabetes.

Do serum hepassocin levels change in women with polycystic ovary syndrome?

BackgroundInsulin resistance is common in polycystic ovary syndrome (PCOS), especially in obese patients. Hepassocin is a peptid marker which increases in obesity and insulin resistance. ObjectiveWe aimed to investigate hepassocin levels in patients with PCOS in this study. MethodsThis prospective case-control study was conducted with a total of 60 patients with PCOS and age-matched 30 healthy women with body mass index < 30. Patients with PCOS were classified as obese PCOS and non-obese PCOS according to their BMI. Hepassocin levels were measured by using a commercially available enzyme-linked immunosorbent assay (ELISA) kit. A multivariate linear regression analysis was used to determine independent factors related to hepassocin levels. ResultsHepassocin levels of the obese-PCOS group were found significantly higher than non-obese PCOS and control group (6.95 ± 3.59, 2.69 ± 2.51, 2.66 ± 2.22, respectively, p < 0.001). There was no significant difference in hepassocin levels between control and non-obese PCOS group (p = 0.99). Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) was independently associated with hepassocin concentrations after adjusting for age, low density lipoprotein C (LDL-C), high density lipoprotein C (HDL-C), triglyceride (TG), total testosterone, dehydroepiandrosterone sulfate (DHEA-S), and C reactive protein (CRP). ConclusionObese patients with PCOS exhibited high serum levels of hepassocin. HOMA-IR index was found as the independent variable associated with high levels of hepassocin. Hepassocin can be used as a simple and easy way of detecting insulin resistance in obese patients with PCOS.

Role of serum adropin measurement in the assessment of insulin resistance in obesity

Obesity has recently been mentioned as a metabolic pandemic in developed and developing countries and is an important known risk factor for type 2 diabetes and cardiovascular diseases. The main...

Relationship between Vitamin D level and Insulin Resistance According to Obesity Level

Introduction: Obesity and metabolic syndrome are universal health problems. There is increasing evidence that vitamin D deficiency is a risk factor in the development of insulin resistance(IR). This study was aimed to investigate the relationship between vitamin D level and IR in obese patients.&#x0D; Method: The study included 95 adult, obese patients, without a history of hypertension, diabetes mellitus, and hyperlipidemia. Fasting blood glucose, insulin, 25-OH-vitamin D, and serum lipid levels were measured and the HOMA-IR level was calculated. The patients were divided into 3 groups according to their obesity level.&#x0D; Results: Seventy-eight (82.1%) of patients were female and vitamin D deficiency was found in 77.9% of the patients. The median HOMA-IR level of the group with and without vitamin D deficiency was 3.57, and 2.39, respectively (p = 0.029). &#x0D; There weren't any significant differences in gender, BMI, and vitamin D levels between the groups with /without IR.&#x0D; No difference was found between obesity level groups in terms of age, gender, and vitamin D level. However, while insulin level and IR level increased significantly in morbid obese patients, this relationship could not be demonstrated in super-obese patients. &#x0D; Conclusion: This study is the first study investigating the relationship between vitamin D-HOMA-IR in morbid and super obese patients. No statistically significant linear correlation was found between vitamin D and HOMA-IR level, but vitamin D deficiency was more common in the group with IR. Additional studies are needed to explain the relationship between the level of obesity and the effect of vitamin D on IR.