Insulin Resistance In Type Research Articles

Acupuncture for Treating Hypertension and Type 2 Diabetes Mellitus as Comorbidities in Patients with COVID-19.

Objective: The world is experiencing challenging times caused by spread of the Coronavirus Disease 2019 (COVID-19), which is caused by infection with Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). Hypertension and type 2 diabetes mellitus are the most prevalent comorbidities of COVID-19. This review discusses several studies that showed the effect of acupuncture on hypertension and type 2 diabetes mellitus, and that discussed the mechanism of acupuncture, points used, and treatment strategies. Method: Literature was searched for studies published from 2016 to 2020 on how acupuncture affects hypertension and type 2 diabetes mellitus on the Google Scholar and PubMed databases using the keywords acupuncture, diabetes mellitus, and hypertension. Randomized clinical trials on human subjects, studies that measured systolic blood pressure (SBP) and diastolic blood pressure (DBP) as outcomes, and studies that measured plasma glucose level as the outcome were included. Studies that did not include clinical effects of acupuncture were excluded. Results: Studies on hypertension (n = 2) and type 2 diabetes mellitus (n = 2) were found. These studies suggested that acupuncture might be able to reduce SBP and DBP, fasting plasma glucose level, oral glucose tolerance, and random blood glucose level. Conclusions: Preliminary studies have suggested that acupuncture might reduce BP in hypertension and reduce blood sugar and insulin resistance in type 2 diabetes mellitus. More research is required to demonstrate if acupuncture is a useful adjunct for treating hypertension and type 2 diabetes mellitus as comorbidities of COVID-19.

"Adjusting Internal Organs and Dredging Channel" Electroacupuncture Ameliorates Insulin Resistance in Type 2 Diabetes Mellitus by Regulating the Intestinal Flora and Inhibiting Inflammation.

IntroductionTraditional Chinese acupuncture has been demonstrated to be beneficial for treatment of type 2 diabetes mellitus (T2DM). The mechanism of acupuncture on T2DM is crucial for their biological activity as well as their usefulness as tools in biology and medicine. However, its mechanism is poorly understood.MethodsIn an effort to explore the mechanism, eight db/db mice (a type of spontaneous T2DM mouse) were treated with adjusting internal organs and dredging channel electroacupuncture (AODCEA) for 2 weeks. Another eight db/db mice were fed as T2DM group (T2DMG), and eight db/m mice were set as normal control group (NCG). Lipopolysaccharide (LPS), interleukin-6 (IL-6), and diabetes-related indicators, such as fasting blood glucose (FBG) and triglyceride (TG), were detected by enzyme-linked immune sorbent assay (ELISA). The V4 region of 16S rRNA gene was analyzed by Illumina sequencing to evaluate the effect of AODCEA on intestinal flora. The amount of short-chain fatty acids (SCFAs) in the feces were determined by gas chromatography-mass spectrometry (GC-MS).ResultsOur results indicate that AODCEA treatment can reduce diabetes-related indicators. We observed the increased probiotics such as Blautia and Lactobacillus and decreased opportunist pathogens (Alistipes, Helicobacter, Prevotella) by AODCEA interventions. Importantly, the total amount of SCFAs in the feces of T2DM mice was promoted by AODCEA. Finally, obviously alleviated systemic inflammation was exhibited through AODCEA treatment by detection of lipopolysaccharide (LPS) and interleukin-6 (IL-6) in serum.ConclusionAODCEA can reshape the structure of intestinal flora, which can increase intestinal SCFAs, affect the circulating LPS level, and reduce the inflammatory response.

Abstract #1003783: COVID-19 Telehealth Model for Severe Insulin Resistant Type 2 Diabetes using Medically Tailored Meals

Los Angeles County + University Southern California (LAC+USC) Medical Center, the largest county medical center in Los Angeles, provides care to some of the most vulnerable and complex underserved patients in the United States. One population of complex patients commonly referred to the LAC+USC Complex Diabetes Clinic is the severe insulin resistance type 2 diabetes group, defined by patients requiring greater than the total daily insulin dose of 200 units. Most interventions for this group use more potent insulin concentrations such as U-500 or cocktails of more expensive drugs.

Visceral adiposity index and atherogenic index of plasma: Simple markers of insulin resistance in type 2 diabetic patients

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Insulin resistance in type 1 diabetes managed with metformin (INTIMET): Study protocol of a double-blind placebo-controlled, randomised trial.

Insulin resistance is an under-recognised metabolic defect and cardiovascular risk factor in Type 1 diabetes. Whether metformin improves hepatic, muscle or adipose tissue insulin sensitivity has not been studied in adults with Type 1 diabetes. We initiated the INTIMET study (INsulin resistance in Type 1 diabetes managed with METformin), a double-blind randomised, placebo-controlled trial to measure the effect of metformin on tissue-specific insulin resistance in adults with Type 1 diabetes. We will study 40 adults aged 20-55years with Type 1 diabetes (HbA1c 80mmol/mol [9.5%], fasting C-peptide <0.3nmol/L) and 20 age-, gender- and body mass index (BMI)-matched controls. Insulin sensitivity will be determined by the two-step hyperinsulinaemic-euglycaemic clamp method with deuterated glucose to document liver, muscle and adipose insulin sensitivity. Subjects with Type 1 diabetes will be randomised to metformin extended-release 1500mg daily or matched placebo for 26weeks. The primary outcome is change in hepatic insulin sensitivity, assessed by change in basal rate of appearance (Ra) of glucose and suppression of endogenous glucose production (EGP) during the low-dose stage of the clamp. The INTIMET study is the first clinical trial to quantify the impact of metformin on liver, muscle and adipose insulin resistance in adults with Type 1 diabetes. This study may identify factors that predict an individual's response to metformin in Type 1 diabetes. ACTRN12619001440112.

Comparative effects of metformin and glibenclamide on the redox balance in type 2 diabetic patients

It is known that there is a strong association between oxidative stress and insulin resistance in type 2 diabetes mellitus (T2DM). Although the role of glibenclamide in diabetes treatment has been evaluated, there is only limited evidence about its antioxidant effects in diabetic patients. Moreover, previous studies showed discrepant results regarding the effects of metformin on antioxidant/ oxidant parameters in type 2 diabetic patients. The present study aimed to evaluate the effects of metformin versus glibenclamide on oxidative stress biomarkers, represented by serum malondialdehyde (MDA), nonenzymatic, and enzymatic antioxidants in type 2 diabetic patients. Forty-six patients with T2DM participated in this study and categorized into 3 groups, Group A included 17 newly diagnosed diabetic patients, group B included 15 diabetic patients received metformin monotherapy (1000 mg/day) for up to 1 year and group C included 14 diabetic patients received glibenclamide monotherapy (5 mg/day) for up to 1 year. Serum MDA, catalase (CAT), vitamin C, E, and reduced glutathione (GSH) were measured. We found significantly lower concentrations of MDA and significantly higher antioxidant levels (CAT, GSH, vitamin C, and E) in the metformin-treated group compared to the glibenclamide counterpart. Our data confirmed that metformin has a more beneficial effect on oxidant/antioxidant status compared to glibenclamide, therefore, provides protection against reactive oxygen species (ROS) induced oxidative damage during diabetes.

Defining the underlying defect in insulin action in type 2 diabetes.

Insulin resistance is one of the earliest defects in the pathogenesis of type 2 diabetes. Over the past 50years, elucidation of the insulin signalling network has provided important mechanistic insights into the abnormalities of glucose, lipid and protein metabolism that underlie insulin resistance. In classical target tissues (liver, muscle and adipose tissue), insulin binding to its receptor initiates a broad signalling cascade mediated by changes in phosphorylation, gene expression and vesicular trafficking that result in increased nutrient utilisation and storage, and suppression of catabolic processes. Insulin receptors are also expressed in non-classical targets, such as the brain and endothelial cells, where it helps regulate appetite, energy expenditure, reproductive hormones, mood/behaviour and vascular function. Recent progress in cell biology and unbiased molecular profiling by mass spectrometry and DNA/RNA-sequencing has provided a unique opportunity to dissect the determinants of insulin resistance in type 2 diabetes and the metabolic syndrome; best studied are extrinsic factors, such as circulating lipids, amino acids and other metabolites and exosomal microRNAs. More challenging has been defining the cell-intrinsic factors programmed by genetics and epigenetics that underlie insulin resistance. In this regard, studies using human induced pluripotent stem cells and tissues point to cell-autonomous alterations in signalling super-networks, involving changes in phosphorylation and gene expression both inside and outside the canonical insulin signalling pathway. Understanding how these multi-layered molecular networks modulate insulin action and metabolism in different tissues will open new avenues for therapy and prevention of type 2 diabetes and its associated pathologies.

Beneficial effect of omarigliptin on diabetic patients with non-alcoholic fatty liver disease/non-alcoholic steatohepatitis

BackgroundDipeptidyl peptidase 4 (DPP4) is a serine exopeptidase able to inactivate various oligopeptides, and also a hepatokine. Hepatocyte-specific overexpression of DPP4 is associated with hepatic insulin resistance and liver steatosis.MethodWe examined whether weekly DPP4 inhibitor omarigliptin (OMG) can improve liver function as well as levels of inflammation and insulin resistance in type 2 diabetic patients with non-alcoholic fatty liver disease (NAFLD). Further, we investigated the effects of OMG in a diabetic patient with biopsy-confirmed nonalcoholic steatohepatitis (NASH).ResultsIn NAFLD patients, OMG significantly decreased levels of aminotransferase, aspartate aminotransferase, gamma-glutamyl transpeptidase, homeostatic model assessment of insulin resistance (HOMA-IR), and high-sensitivity C-reactive protein (hsCRP), while no significant change was seen in hemoglobin A1c or body mass index. In the NASH patient, liver function improved markedly, and levels of the hepatic fibrosis marker FIB-4 decreased in parallel with HOMA-IR and hsCRP. Slight but clear improvements in intrahepatic fat deposition and fibrosis appeared to be seen on diagnostic ultrasonography.ConclusionWeekly administration of the DPP4 inhibitor OMG in ameliorating hepatic insulin resistance may cause beneficial effects in liver with NAFLD/NASH.

Adipose tissue cadmium concentrations as a potential risk factor for insulin resistance and future type 2 diabetes mellitus in GraMo adult cohort.

Adipose tissue has been recently highlighted as a promising matrix for evaluation of cadmium's (Cd) long-term exposure although not frequently considered in epidemiological studies. The association between Cd exposure and type 2 Diabetes Mellitus (T2DM) remains unclear. This work aimed to explore the association between adipose tissue Cd levels and T2DM incidence over a 16-year follow-up in an adult cohort from Southern Spain considering smoking status. We also performed complementary cross-sectional analyses focused on subclinical markers of glucose homeostasis at recruitment. Clinical information was obtained from hospital databases. Socio-demographic characteristics, lifestyle and diet were collected by face-to-face interviews. Homeostatic model assessment (HOMA) values of insulin sensitivity/resistance and β-cell function were calculated using fasting serum glucose, insulin, and C-peptide levels at recruitment. Adipose tissue Cd concentrations were quantified by inductively coupled plasma mass spectrometry. Statistical analyses were performed by means of Cox-regression and multivariable linear regression models. Participants in the 4th quartile (Q4) of Cd concentrations showed a non statistically-significant increased T2DM risk (Hazard Ratio (HR) Q4 vs Q1: 1.97; 95% Confidence Interval (CI): 0.69, 5.66). This association was particularly strong and suggestive in current smokers (HR: 2.19; 95% CI: 0.98, 4.98). Interestingly, smokers in the 2nd tertile (T2) of adipose tissue Cd levels showed increased log-transformed insulin resistance (beta T2 vs T1: 0.52; 95% CI: 0.07, 0.97), as well as higher log-transformed insulin levels (beta T2 vs T1: 0.52; 95% CI: 0.08, 0.95). We found evidences supporting that Cd exposure, particularly from tobacco smoking, could be a risk factor for T2DM. In addition, our results support the potential relevance of adipose tissue as a matrix for Cd exposure assessment.

Gamma-aminobutyric acid attenuates insulin resistance in type 2 diabetic patients and reduces the risk of insulin resistance in their offspring

The role of gamma-aminobutyric acid (GABA) in attenuates insulin resistance (IR) in type 2 diabetic (T2D) patients and the reduction of the risk of IR in their offspring, and the function of GLUT4, IRS1 and Akt2 genes expression were investigated. T2D was induced by high fat diet and 35 mg/kg of streptozotocin. The male and female diabetic rats were then divided into three groups: CD, GABA, and insulin. NDC group received a normal diet. All the animals were studied for a six-month. Their offspring were just fed with normal diet for four months. Blood glucose was measured weekly in patients and their offspring. Intraperitoneal glucose tolerance test (IPGTT), urine volume, and water consumption in both patients and their offspring were performed monthly. The hyperinsulinemic euglycemic clamp in both patients and their offspring was done and blood sample collected to measure Hemoglobin A1c (HbA1c). IRS1, Akt and GLUT4 gene expressions in muscle were evaluated in all the groups. GABA or insulin therapy decreased blood glucose, IPGTT, and HbA1c in patients and their offspring compared to DC group. They also increased GIR in patients and their offspring. IRS1, Akt and GLUT4 gene expressions improved in both patients in comparison with DC group. GABA exerts beneficial effects on IRS1 and Akt gene expressions in GABA treated offspring. GABA therapy improved insulin resistance in diabetic patients by increasing the expression of GLUT4. It is also indirectly able to reduce insulin resistance in their offspring possibly through the increased gene expressions of IRS1 and Akt.

Mechanistic Insights into Side Effects of Troglitazone and Rosiglitazone Using a Novel Inverse Molecular Docking Protocol.

Thiazolidinediones form drugs that treat insulin resistance in type 2 diabetes mellitus. Troglitazone represents the first drug from this family, which was removed from use by the FDA due to its hepatotoxicity. As an alternative, rosiglitazone was developed, but it was under the careful watch of FDA for a long time due to suspicion, that it causes cardiovascular diseases, such as heart failure and stroke. We applied a novel inverse molecular docking protocol to discern the potential protein targets of both drugs. Troglitazone and rosiglitazone were docked into predicted binding sites of >67,000 protein structures from the Protein Data Bank and examined. Several new potential protein targets with successfully docked troglitazone and rosiglitazone were identified. The focus was devoted to human proteins so that existing or new potential side effects could be explained or proposed. Certain targets of troglitazone such as 3-oxo-5-beta-steroid 4-dehydrogenase, neutrophil collagenase, stromelysin-1, and VLCAD were pinpointed, which could explain its hepatoxicity, with additional ones indicating that its application could lead to the treatment/development of cancer. Results for rosiglitazone discerned its interaction with members of the matrix metalloproteinase family, which could lead to cancer and neurodegenerative disorders. The concerning cardiovascular side effects of rosiglitazone could also be explained. We firmly believe that our results deepen the mechanistic understanding of the side effects of both drugs, and potentially with further development and research maybe even help to minimize them. On the other hand, the novel inverse molecular docking protocol on the other hand carries the potential to develop into a standard tool to predict possible cross-interactions of drug candidates potentially leading to adverse side effects.

ПСИХОЛОГИЧЕСКИЕ АСПЕКТЫ ПРИМЕНЕНИЯ МДМ-ТЕРАПИИ У ПАЦИЕНТОВ С МЕТАБОЛИЧЕСКИМ СИНДРОМОМ ПРИ ПРОТЕЗИРОВАНИИ ОРТОПЕДИЧЕСКИМИ КОНСТРУКЦИЯМИ С ОПОРОЙ НА ДЕНТАЛЬНЫЕ ИМПЛАНТАТЫ

The article analyzes the practical results of the study of the effect of the method of physiotherapeutic influence on the effectiveness and timing of treatment and recovery of patients with metabolic disorders who need restorative dental treatment and prosthetics in order to compensate for secondary adentia in the form of incomplete dentition. The study involved three groups of patients (two experimental and one control) with a diagnosis of insulin-resistant type II diabetes mellitus and moderate severity. The main type of specialized dental treatment was the tactic of edentulous compensation by means of prosthetic constructions placed in the oral cavity in support of previously installed dental implants. Throughout the study, special attention was paid to monitoring and analyzing various aspects of the psychoemotional state of prosthetic patients, disturbed mainly due to dental stress, the development of which was aggravated by metabolic disorders already existing in patients of this category. Studies of the psychoemotional state of the prosthetic patients were carried out at all stages of preclinical assessment and diagnosis, as well as during the intraclinical period: initial examination, preparation for the installation of implants and prosthetic structures, as well as their subsequent general and functional rehabilitation, as well as in parallel in all groups in which study. The primary empirical generalization of significant clinical information of a psycho-somatic and purely psychological nature was carried out in the direction of determining the depth and duration of the action of correlates of prevention and leveling of the emerging dental stress with the main neurohumoral factors that provide such important characteristics of osseointegration in the postoperative period as the engraftment of installed dental implants and their subsequent stability as a support for the placement and installation of prosthetic dental structures. There was an increased complexity of prosthetics due to the presence of manifestations of osteopenic syndrome as a consequence of metabolic disorders developed in patients. The study assesses the possible improvement in the prognosis of this type of dental treatment precisely as a consequence of the use of the mesodiencephalic modulation method, which makes it possible to facilitate the solution of a number of problems facing the clinician, mainly of a psychological nature.

Impact of Hepatitis C virus Infection and direct-acting Oral Antiviral Drugs on glycaemic state in Type 2 Diabetic Patients

Background: Diabetes mellitus (DM) is strongly associated with chronic hepatitis C virus (HCV) infection. This work aimed to estimate the impact of Hepatitis C virus infection on glycaemic state and insulin resistance in type 2 Diabetic patients, and evaluate the effect of direct-acting oral antiviral treatment on the glycaemic state and insulin resistance in type 2 Diabetic patients. Methods: The study was performed on (40 patients) with Type 2 Diabetes who were infected by Hepatitis C Virus and took Direct-acting Oral Antiviral Drugs. The study also included (10 patients) who had Type 2 Diabetes and HCV infection serving as control group. All patients and control were subjected to thorough history taking, clinical examination, and lab. investigations as FBG, PP and HBA1c , Serum fasting Insulin level, And HOMA-IR, HCVab – HBsAg – HIVab, CBC, SGOT, SGPT, Serum Albumin and Bilirubin, PCR for HCV RNA, and Abdominal US. Results: DAAs-based eradication of HCV is associated with improved glycemic control in patients with type 2 diabetes as evidenced by a significant reduction of mean FBG, Fasting insulin, HbA1c, and HOMA IR. There was a positive correlation between the treatment of HCV infection and the reduction of anti-diabetic drugs used in the studied patients. Conclusion: DAAs-based eradication of HCV is associated with improved glycemic control in patients with type 2 diabetes.

L-lysine supplementation improved glycemic control, decreased protein glycation, and insulin resistance in type 2 diabetic patients

Lysine treatment decreased diabetic complications associated with type 2 diabetes in the rat models of diabetes and in vitro. Herein, in a single-evaluator–blinded, randomized clinical trial, we investigated the effect of L-Lysine (Lys) intervention in type 2 diabetic patients. Two groups of type 2 diabetic patients (15 females and 10 males in each group) who were under treatment with glibenclamide and metformin underwent a short term (3 months), trial. The test group was orally administered with 3 g/day of Lys. Clinical and biochemical parameters of all patients were measured prior to and after the experimental period and were statistically analyzed. Among the serum parameters, FBS, insulin, HOMA-IR, HSP 70, LCAT, PON1, AOPP, and FRAP improved significantly in the test group. A significant decrease in HbA1c and urine glucose accompanying with positive correlations between HbA1c and FBS, fructosamine and both FBS and HbA1c, HOMA with both insulin and FBS, and FBS with urine glucose indicates that Lys prevents diabetes complications. There were no significant changes in the liver and kidney function tests indicating no toxicity of Lys for patients. In conclusion, Lys inhibited protein glycation, improved glycemic control, and increased antioxidant markers in type 2 diabetic patients; thus, it could be suggested for combinatorial therapy of diabetes with oral hypoglycemic agents to protect against vascular risk factors and other diabetic complications.

NAFLD, Insulin Resistance, and Diabetes Mellitus Type 2.

Nonalcoholic fatty liver disease is a condition defined by fat accumulation in hepatocytes not promoted by excessive alcohol consumption. It is highly prevalent and is strongly associated with insulin resistance, metabolic syndrome, and diabetes type II. Insulin resistance plays a crucial role in the multifactorial etiopathogenesis of this condition leading to accumulation of free fatty acids in the liver cells, thus causing lipotoxicity, inflammation, and fibrosis. In this review, we will focus on currently known pathogenesis of nonalcoholic fatty liver disease. Numerous investigation strategies are available to establish the diagnosis, from biochemical markers and ultrasound to various molecular and advanced imaging techniques and liver biopsy. Prevention is crucial. However, effective and promising therapies are strongly demanded.

Brown Adipose Tissue and Its Role in Insulin and Glucose Homeostasis.

The increased worldwide prevalence of obesity, insulin resistance, and their related metabolic complications have prompted the scientific world to search for new possibilities to combat obesity. Brown adipose tissue (BAT), due to its unique protein uncoupling protein 1 (UPC1) in the inner membrane of the mitochondria, has been acknowledged as a promising approach to increase energy expenditure. Activated brown adipocytes dissipate energy, resulting in heat production. In other words, BAT burns fat and increases the metabolic rate, promoting a negative energy balance. Moreover, BAT alleviates metabolic complications like dyslipidemia, impaired insulin secretion, and insulin resistance in type 2 diabetes. The aim of this review is to explore the role of BAT in total energy expenditure, as well as lipid and glucose homeostasis, and to discuss new possible activators of brown adipose tissue in humans to treat obesity and metabolic disorders.

Circulating and visceral adipose tissue miR-330-3p is associated with insulin resistance in Type II Diabetes Mellitus

Circulating and visceral adipose tissue miR-330-3p is associated with insulin resistance in Type II Diabetes Mellitus

Identification of Three Significant Genes Associated with Immune Cells Infiltration in Dysfunctional Adipose Tissue-Induced Insulin-Resistance of Obese Patients via Comprehensive Bioinformatics Analysis.

Background Low-grade chronic inflammation in dysfunctional adipose tissue links obesity with insulin resistance through the activation of tissue-infiltrating immune cells. Numerous studies have reported on the pathogenesis of insulin-resistance. However, few studies focused on genes from genomic database. In this study, we would like to explore the correlation of genes and immune cells infiltration in adipose tissue via comprehensive bioinformatics analyses and experimental validation in mice and human adipose tissue. Methods Gene Expression Omnibus (GEO) datasets (GSE27951, GSE55200, and GSE26637) of insulin-resistant individuals or type 2 diabetes patients and normal controls were downloaded to get differently expressed genes (DEGs), and GO and KEGG pathway analyses were performed. Subsequently, we integrated DEGs from three datasets and constructed commonly expressed DEGs' PPI net-works across datasets. Center regulating module of DEGs and hub genes were screened through MCODE and cytoHubba in Cytoscape. Three most significant hub genes were further analyzed by GSEA analysis. Moreover, we verified the predicted hub genes by performing RT qPCR analysis in animals and human samples. Besides, the relative fraction of 22 immune cell types in adipose tissue was detected by using the deconvolution algorithm of CIBERSORT (Cell Type Identification by Estimating Relative Subsets of RNA Transcripts). Furthermore, based on the significantly changed types of immune cells, we performed correlation analysis between hub genes and immune cells. And, we performed immunohistochemistry and immunofluorescence analysis to verify that the hub genes were associated with adipose tissue macrophages (ATM). Results Thirty DEGs were commonly expressed across three datasets, most of which were upregulated. DEGs mainly participated in the process of multiple immune cells' infiltration. In protein-protein interaction network, we identified CSF1R, C1QC, and TYROBP as hub genes. GSEA analysis suggested high expression of the three hub genes was correlated with immune cells functional pathway's activation. Immune cell infiltration and correlation analysis revealed that there were significant positive correlations between TYROBP and M0 macrophages, CSF1R and M0 macrophages, Plasma cells, and CD8 T cells. Finally, hub genes were associated with ATMs infiltration by experimental verification. Conclusions This article revealed that CSF1R, C1QC, and TYROBP were potential hub genes associated with immune cells' infiltration and the function of proinflammation, especially adipose tissue macrophages, in the progression of obesity-induced diabetes or insulin-resistance.

Could insulin receptor H1085H C > T single nucleotide polymorphism predict insulin resistance in type 2 diabetic and chronic hepatitis C virus patients in Egypt?

BackgroundInsulin-receptor (INSR) is an α2β2 heterotetramer disulfide-linked trans-membrane glycoprotein and a family member of tyrosine kinase receptors. It mediates the pleiotropic actions of insulin regulating glucose homeostasis. It is encoded by a single gene: INSR gene. The INSR gene comprises 22 exons. Exons 17–22 encode the tyrosine kinase domain, and mutations in this region impair the function of the insulin receptor that may cause insulin resistance and hyperinsulinemia. Single nucleotide polymorphism with C > T substitution at His 1058 position of INSR (rs 1799817) located in exon 17 was considered to be involved in insulin resistance. Insulin receptor might be counter-regulated by degradation, differential expression, or modification by phosphorylation in cells expressing HCV core protein. HCV infection eventually leads to liver steatosis and fibrosis, increased oxidative stress, and peroxidation, all of which trigger a cascade of inflammatory responses, thus contributing to the development of insulin resistance. The present retrospective case-control aimed to study INSR H1085H C > T (rs 1799817) SNP in Egyptian patients suffering from chronic HCV infection with DM. The current study was conducted on two hundred and two participants of 100 males and 102 females, divided as follows: the control group (group I) included 50 apparently healthy volunteers of comparable age, sex, and socioeconomic status as patients groups, group II included 50 type 2 DM patients without HCV infection, group III included 52 chronic HCV infected patients without DM, and group IV included 50 HCV patients with DM.ResultsHOMA-IR and QUICKI index was significantly higher in the patient groups (groups II, III, and IV) than in controls (P < 0.001, P = 0.019, and P < 0.001, respectively). It was significantly lower in patients of group III than in patients of groups II and IV with P < 0.001 for both. DM patient group without HCV infection (group II) and HCV with DM (group IV) showed a significant decrease in CC genotypes and a significant increase in TT genotypes than the controls (P < 0.001, P = 0.018, respectively). HCV patients with DM (group IV) had the highest frequency of heterozygous genotype (CT) (50%). HCV-infected patients with T2DM (group IV) also showed a significantly higher frequency of minor allele (T) (35%) than controls (20%), and a lower frequency of the wild allele (C) (65%) than controls (80%).ConclusionThe mutant allele “T” of INSR H1085H C > T (rs 1799817) SNP might be associated with an increased risk of developing insulin resistance and T2DM.

The relationship between serum irisin levels and erectile dysfunction in diabetic men (irisin and erectile dysfunction in diabetic patients)

Irisin is an exercise-induced myokine that alleviates endothelial dysfunction and reduces insulin resistance in type 2 diabetes mellitus. We conducted this cross-sectional prospective study to determine the association of serum irisin levels and erectile dysfunction in type 2 diabetic patients. We compared 34 diabetic patients with erectile dysfunction with 30 diabetic patients without erectile dysfunction. In our study, serum irisin levels were found to be statistically significantly higher in diabetic patients without erectile dysfunction compared to those with erectile dysfunction (p=.016) and according to correlation analysis, irisin levels had a significantly negative correlation with the serum HbA1C value (r=-.294, p=.018). Based on the results of our study, we think that this molecule can be used in the diagnosis or treatment of erectile dysfunction in diabetic patients, if these findings are supported by larger studies.