scholarly journals Role of insulin-degrading enzyme (IDE) in diabetes mellitus and insulin resistance

2018 ◽  
Author(s):  
Pablo Villa Pérez
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Insulin Degrading Enzyme ◽  
Degrading Enzyme

scholarly journals Magnesium, Little Known But Possibly Relevant: A Link between NASH and Related Comorbidities

Biomedicines ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 125
Author(s):  
Jorge Simón ◽  
Teresa Cardoso Delgado ◽  
Luis Alfonso Martinez-Cruz ◽  
Maria Luz Martínez-Chantar
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Inflammatory Process ◽  
Fibrotic Response ◽  
Hepatic Lipid Accumulation ◽  
Root Cause ◽  
Worldwide Population ◽  
Global Health Problem

Non-alcoholic steatohepatitis (NASH) is characterized by an abnormal hepatic lipid accumulation accompanied by a necro-inflammatory process and a fibrotic response. It comprises from 10% to 30% of cases of patients with non-alcoholic liver disease, which is a global health problem affecting around a quarter of the worldwide population. Nevertheless, the development of NASH is often surrounded by a pathological context with other comorbidities, such as cardiovascular diseases, obesity, insulin resistance or type 2 diabetes mellitus. Dietary imbalances are increasingly recognized as the root cause of these NASH-related comorbidities. In this context, a growing concern exists about whether magnesium consumption in the general population is sufficient. Hypomagnesemia is a hallmark of the aforementioned NASH comorbidities, and deficiencies in magnesium are also widely related to the triggering of complications that aggravate NASH or derived pathologies. Moreover, the supplementation of this cation has proved to reduce mortality from hepatic complications. In the present review, the role of magnesium in NASH and related comorbidities has been characterized, unraveling the relevance of maintaining the homeostasis of this cation for the correct functioning of the organism.

scholarly journals Predictors of Insulin Resistance in Obesity and Type 2 Diabetes Mellitus - The Role of Magnesium

2017 ◽  
Vol 06 (04) ◽  
Author(s):  
Soetkin Milbouw ◽  
Julie Verhaegen ◽  
An Verrijken ◽  
Benedicte Y De Winter ◽  
Luc F Van Gaal ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus

ID: 79: INSULIN TREATMENT INCREASES MICROVESICULAR INSULIN-DEGRADING ENZYME IN DIABETES

2016 ◽  
Vol 64 (4) ◽  
pp. 926.2-927
Author(s):  
MV Purbaugh ◽  
CV Desouza ◽  
R Heineman ◽  
RG Bennett ◽  
FG Hamel
Keyword(s):  
Insulin Resistance ◽  
Western Blot ◽  
Insulin Treatment ◽  
Statistical Significance ◽  
Diabetic Group ◽  
Insulin Clearance ◽  
Diabetic Patients ◽  
Insulin Degrading Enzyme ◽  
Healthy Group ◽  
Degrading Enzyme

Insulin-degrading enzyme (IDE) in the blood may play a role in insulin clearance, thus decreased IDE activity could contribute to hyperinsulinemia and possibly type 2 diabetes mellitus (T2DM). We hypothesized that decreased IDE in plasma may be associated with obesity and/or T2DM. We recruited non-obese (BMI<30, no significant disease), obese (BMI>30) and diabetic (T2DM; ICD-9 code) patients and obtained fasting blood samples. Microvesicular (containing exosomes) and soluble fractions were isolated from plasma by ultracentrifugation Insulin degrading activity was assayed by trichloroacetic acid precipitation of 125I-iodoinsulin (TCA assay), while IDE protein was detected by Western blotting. Differences were analyzed by ANOVA with a Bonferroni posttest. There was no IDE present in the soluble fraction as confirmed by both the TCA assay and Western blot. IDE activity was present in the microvesicular fraction, and the Western blot intensity correlated significantly with activity (p=.01). However, there were no significant differences in IDE activity or protein levels among the 3 groups. We then conducted a post hoc analysis byseparating the non-obese and obese patients into two groups: a healthy group (HbA1c<6) and a pre-diabetic group (HbA1c of 6.0–6.4). We also separated the diabetic patients into two groups: a diabetic group and an insulin-treated group. Although there was no statistical difference in IDE activity among the healthy group, pre-diabetic and diabetic groups, the latter two groups showed a trend toward decreased IDE activity. Interestingly, in patients receiving insulin treatment, the effect of diabetes was reversed, with, increased microvesicular degrading activity compared to the pre-diabetic group (p<0.05) and the diabetic group (p<0.05). The increased IDE activity in the insulin-treated diabetics roughly correlated with the patient's insulin dose, but did not reach statistical significance (r2=.38; p=0.14). We saw no statistically significant correlations of degrading activity with a number of clinical parameters including: fasting glucose; triglycerides, LDL, HDL, age, eGFR, and HbA1c by linear regression. This shows that the microvesicular IDE is not affected by glucose or lipid control. We conclude: A) IDE is present in the blood, but does not significantly contribute to insulin clearance because the microvesicular fraction showed no insulin clearance unless they were first frozen and thawed. This freezing and thawing process most likely allowed the microvesicular membranes to rupture releasing the enzyme. B) enzymatically active IDE is associated with a fraction consistent with exosomes and may be decreased in pre-diabetes and diabetes; and C) insulin treatment increases microvesicular IDE. IDE in the exosomes may serve as a marker for the progression of the pre-diabetic and diabetic disease states independent of glucose control. One could speculate that inflammation and/or insulin resistance result in a decrease of vesicular IDE activity and that insulin treatment reverses this through its anti-inflammatory properties, or by overcoming insulin resistance and increasing insulin signaling.

The role of myokines in the development of insulin resistance in children, with type 1 diabetes mellitus

2021 ◽  
pp. 19-26
Author(s):  
O. Ye. Pashkova ◽  
N. I. Chudova ◽  
O. S. Litvinenko
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Type 1 Diabetes ◽  
Muscle Strength ◽  
Blood Serum ◽  
Muscle Mass ◽  
Pediatric Patients ◽  
Control Group

The aim — to study the role of myokines in the development of insulin resistance in children with type 1 diabetes mellitus.Materials and methods. Observations involved 68 children with type 1 diabetes mellitus (DM 1), with the mean age 11 to 17 years. Depending on the glycemic controllevel, patients were divided into 3 research groups. The control group consisted of 20 relatively healthy children. Muscle mass, the skeletal muscles index, fat mass and the percentage of fat in the bodywere determined in all patients. The Lovett’s test was used to assess the loss of muscle strength; evaluation of insulin resistance was made based onthe triglyceride­glucose index (TYG). Levels of myostatin, irisin, interleukins ­6 and ­13were measured in blood serum.Results and discussion. It has been established that with deterioration in the level of glycemic controlin DM 1 children, the component redistribution of body composition took place with an increased fat mass proportionand decreased muscle mass. This resulted in the reduced insulin-mediatedabsorption of glucose, that was confirmed by the significant increase in TYG level compared to control group. The analysis of cytokines in the blood serum showed a significant increase in the level of myostatin and interleukin­6 compared with the control group and the tendency to increased levels of the interleukins ­13 and the level of irisin in the blood serum in pediatric patients with DM 1. The increased levels of myostatin in DM 1childrenassociated with an increase in the triglycerides content (r = 0.44, p < 0.05) and raised TYG index (r = 0.33, p < 0.05), testifying theclose correlation between the high myostatin levels and the development of insulin resistance.Conclusions. In children with diabetes mellitus, the reduction of muscle strength and muscle mass take place with a deterioration in the state of glycemic control, accompanying by the development of insulin resistance. The violation of myokines synthesis,along with the chronic hyperglycemia and diabetic myopathy, plays the leading role in the formation of insulin resistance in pediatric patients with DM 1. It is manifested by the increased production of myostatin and interleukin­6 in the absence of activation of irisin and interleukin­13synthesis.

scholarly journals Expression of Dual-Specificity Phosphatase 9 in Placenta and Its Relationship with Gestational Diabetes Mellitus

2019 ◽  
Vol 2019 ◽  
pp. 1-7
Author(s):  
Qiang Wei ◽  
Xiaomin Pu ◽  
Li Zhang ◽  
Yi Xu ◽  
Meifan Duan ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Body Mass Index ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Pregnant Women ◽  
Plasma Glucose ◽  
Mrna Levels ◽  
Gestational Week

Introduction. The aim of the present study was to examine placental levels of DUSP9 mRNA and protein and to investigate the potential role of DUSP9 in the development of gestational diabetes mellitus (GDM). Methods. Placental tissues from pregnant women with GDM (n=17) and normal healthy pregnant women (n=16) were collected at delivery. The expression of DUSP9 mRNA in placental tissue was analyzed by real-time PCR, while the expression of DUPS9 protein was evaluated by immunohistochemistry and western blot. Differences in the expression levels of DUSP9 mRNA and protein between the two groups were assessed, as well as potential correlations between DUSP9 mRNA expression levels and relevant clinical indicators. Results. Blood glucose levels were significantly higher in the GDM group than in the control group, based on an oral glucose tolerance test. DUSP9 protein was expressed in the placental cytotrophoblasts in both groups, and placental levels of DUSP9 protein and mRNA were significantly higher in women with GDM. Placental DUSP9 mRNA levels in all 33 women correlated moderately with delivery gestational week (R=0.465, P=0.006), fasting plasma glucose (R=0.350, P=0.046), 1-hour postload plasma glucose (R=0.363, P = 0.038), and 2-hour postload plasma glucose (R=0.366, P=0.036), but not with maternal age, preconception body mass index, prenatal body mass index, or neonatal birth weight. Multiple linear regression analysis indicated that delivery gestational week was an influence factor of DUSP9 mRNA levels (β1=0.026, P<0.05). Conclusions. DUSP9 upregulation in the placenta of GDM pregnant women may promote insulin resistance, which may correlate with the occurrence of GDM. But there is still possibility that DUSP9 upregulation was the results of insulin resistance and/or hyperglycemia. Further research is needed to explore the role of DUSP9 in GDM.

scholarly journals The Role of Metabolic Factors in Renal Cancers

2020 ◽  
Vol 21 (19) ◽  
pp. 7246
Author(s):  
Jacek Rysz ◽  
Beata Franczyk ◽  
Janusz Ławiński ◽  
Robert Olszewski ◽  
Anna Gluba-Brzózka
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Malignant Tumours ◽  
Metabolic Factors ◽  
Lipid Disorders ◽  
Igf System ◽  
Low Body Mass Index ◽  
The Impact

An increasing number of evidence indicates that metabolic factors may play an important role in the development and progression of certain types of cancers, including renal cell carcinoma (RCC). This tumour is the most common kidney cancer which accounts for approximately 3–5% of malignant tumours in adults. Numerous studies indicated that concomitant diseases, including diabetes mellitus (DM) and hypertension, as well as obesity, insulin resistance, and lipid disorders, may also influence the prognosis and cancer-specific overall survival. However, the results of studies concerning the impact of metabolic factors on RCC are controversial. It appears that obesity increases the risk of RCC development; however, it may be a favourable factor in terms of prognosis. Obesity is closely related to insulin resistance and the development of diabetes mellitus type 2 (DM2T) since the adipocytes in visceral tissue secrete substances responsible for insulin resistance, e.g., free fatty acids. Interactions between insulin and insulin-like growth factor (IGF) system appear to be of key importance in the development and progression of RCC; however, the exact role of insulin and IGFs in RCC pathophysiology remains elusive. Studies indicated that diabetes increased the risk of RCC, but it might not alter cancer-related survival. The risk associated with a lipid profile is most mysterious, as numerous studies provided conflicting results. Even though large studies unravelling pathomechanisms involved in cancer growth are required to finally establish the impact of metabolic factors on the development, progression, and prognosis of renal cancers, it seems that the monitoring of health conditions, such as diabetes, low body mass index (BMI), and lipid disorders is of high importance in clear-cell RCC.

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