SIRT1 Deacetylates Mitochondrial Trifunctional Enzyme α Subunit to Inhibit Ubiquitylation and Decrease Insulin Resistance

2020 ◽  
Author(s):  
Yan-Mei Wang ◽  
Ting-Lei Huang ◽  
Ying Ma ◽  
Hong-Xia Liu ◽  
Chao Meng ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Α Subunit ◽  
Decrease Insulin Resistance

scholarly journals SIRT1 deacetylates mitochondrial trifunctional enzyme α subunit to inhibit ubiquitylation and decrease insulin resistance

2020 ◽  
Vol 11 (10) ◽  
Author(s):  
Yan-Mei Wang ◽  
Ting-Lei Huang ◽  
Chao Meng ◽  
Jia Zhang ◽  
Ning-Yuan Fang
Keyword(s):  
Insulin Resistance ◽  
Glucose Uptake ◽  
Free Acid ◽  
Critical Role ◽  
Α Subunit ◽  
Chain Reactions ◽  
Insulin Resistant ◽  
Polymerase Chain Reactions ◽  
Reduce Insulin Resistance ◽  
Polymerase Chain

Abstract Dysregulation of free acid metabolism is a major contributor to the development of insulin resistance and diabetes. Mitochondrial trifunctional enzyme subunit (MTPα) has a critical role in fatty acid β-oxidation. However, the association between MTPα and insulin resistance is not definitively known. Here, we aimed to determine how MTPα affects insulin resistance. We tested how MTPα affected glucose uptake in insulin-resistant 3T3-L1 adipocytes and white adipose tissue (WAT) of db/db diabetic mice. We also measured how acetylation and ubiquitylation modifications regulated MTPα activation and stability, using quantitative real-time polymerase chain reactions, immunoblotting, and immunoprecipitation. We found that MTPα overexpression promoted glucose uptake via Glut4 translocation to the plasma membrane in 3T3-L1 adipocytes. Moreover, MTPα upregulation decreased glycemia in db/db mice. Deacetylation increased MTPα protein stability and its ability to reduce insulin resistance. The activation of SIRT1, a major deacetylase, prevented MTPα degradation by decreasing its acetylation in adipocytes. Our study demonstrates a new role for MTPα in reducing insulin resistance. Acetylation and ubiquitylation modifications of MTPα were crucial to regulating its function in glucose metabolism.

Description of the first genetically confirming case with Donahue’s syndrome in Russia

2016 ◽  
Vol 62 (2) ◽  
pp. 42-45
Author(s):  
Yulia V. Tikhonovich ◽  
Oleg A. Malievsky ◽  
Anatoly Tyul'pakov
Keyword(s):  
Insulin Resistance ◽  
Age Of Onset ◽  
Insulin Resistance Syndrome ◽  
Neonatal Diabetes ◽  
Type A ◽  
Β Subunit ◽  
Α Subunit ◽  
Mild Phenotype ◽  
Insr Gene ◽  
Donohue Syndrome

Syndrome Donahue (leprechaunism) is a rare form of neonatal diabetes mellitus associated with INSR gene mutations. There are three types of insulin resistance syndrome: Donohue syndrome, Rabson—Mendenhall syndrome and insulin resistance type A. These syndromes are distinguished from one another by severity of symptoms, age of onset and age of death. Donohue and Rabson—Mendenhall syndromes are associated with biallelic mutations in the α-subunit or/and β-subunit of INSR gene and are characterized by more severe phenotype and poor prognosis. Patients with Donohue syndrome usually die within the first two years of life. Life expectancy of patients with Rabson—Mendenhall syndrome is 5—15 years. Most patients with insulin resistance type A have heterozygous mutations in the β-subunit and demonstrate mild phenotype. Here, we describe the first genetically confirmed case of syndrome Donahue in the Russian Federation.

Telehealth Support to Decrease Insulin Resistance in Overweight and Obese Adolesents: A Pilot Study

2010 ◽  
Vol 46 (2) ◽  
pp. S44
Author(s):  
Alberta S. Kong ◽  
Keri Bolton Oetzel ◽  
Rosemary S. Wold ◽  
Carol Hartenberger ◽  
Betty J. Skipper ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Pilot Study ◽  
Decrease Insulin Resistance

High Maternal DHA Levels in Hawaiian Women Decrease Insulin Resistance

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1404-P
Author(s):  
FERNANDA ALVARADO ◽  
PAI-JONG TSAI ◽  
JUDI MINIUM ◽  
PATRICK CATALANO ◽  
PERRIE O'TIERNEY-GINN
Keyword(s):  
Insulin Resistance ◽  
Decrease Insulin Resistance ◽  
Hawaiian Women

scholarly journals Major Circadian Variations of Glucose Homeostasis in a Patient with Rabson-Mendenhall Syndrome and Primary Insulin Resistance Due to a Mutation(Cys284 → Tyr) in the Insulin Receptor α-Subunit

1997 ◽  
Vol 42 (1) ◽  
pp. 72-77 ◽  
Author(s):  
Christèle Desbois-Mouthon ◽  
Jocelyne Magré ◽  
Jacques Duprey ◽  
Martine Caron ◽  
Marie-José Blivet-Van Eggelpoel ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Receptor ◽  
Glucose Homeostasis ◽  
Circadian Variations ◽  
Α Subunit

scholarly journals Potential Role of the Epithelial Na+ Channel α Subunit Cleavage in the Regulation of Urinary Na+ Excretion During Insulin Resistance

2011 ◽  
Vol 25 (S1) ◽  
Author(s):  
Shaina S. Balayan ◽  
Ruben Rodriguez ◽  
Jose Viscarra ◽  
Akira Nishiyama ◽  
Mouhamed S. Awayda ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Potential Role ◽  
Na Channel ◽  
Α Subunit ◽  
Epithelial Na Channel

scholarly journals The CC genotype of the GNAS T393C polymorphism is associated with obesity and insulin resistance in women with polycystic ovary syndrome

2006 ◽  
Vol 155 (5) ◽  
pp. 763-770 ◽  
Author(s):  
Susanne Hahn ◽  
Ulrich H Frey ◽  
Winfried Siffert ◽  
Susanne Tan ◽  
Klaus Mann ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Oral Glucose ◽  
Allele Carrier ◽  
Metformin Treatment ◽  
Ovary Syndrome ◽  
Α Subunit ◽  
The Common

Objective: Variants in the Gs protein α subunit gene (GNAS1) are known to be involved in the pathogenesis of several endocrine and metabolic disorders. To understand genetic determinants of androgen excess, insulin resistance, and obesity in polycystic ovary syndrome (PCOS), we investigated the effect of the common GNAS1 T393C polymorphism on the phenotype of German PCOS women. Design: Two hundred and seventy-eight PCOS women and 820 Caucasian controls were genotyped for the common T393C polymorphism in GNAS1. To this end, genomic DNA was amplified by PCR with specific oligonucleotides and genotypes were determined using the restriction enzyme FokI. In addition, we evaluated whether the T393C polymorphism had an influence on the response to 6 months metformin treatment in a subgroup of 105 PCOS women. Methods: Anthropometric variables, metabolic parameters including indices of insulin resistance measured by oral glucose tolerance testing, and endocrine biochemical as well as clinical parameters were measured in all PCOS subjects. Results: GNAS1 genotype distributions were not significantly different between PCOS women and controls. In PCOS women, no significant differences in endocrine clinical and biochemical variables were found between the genotypes. However, the C-allele carrier group had significantly higher mean body weight, body mass index, leptin levels, and higher indices of insulin resistance compared with women with GNAS1 TT-genotype. Metformin treatment significantly improved hyperandrogenism, menstrual cyclicity, body weight, and insulin resistance independent of GNAS1 genotype. The major determinant of weight loss was body weight before treatment. Conclusion: The T393C polymorphism is not associated with PCOS in Caucasian women, but may represent a genetic marker for increased susceptibility for obesity in this cohort.

scholarly journals ADAM17 Cleaves the Insulin Receptor α‐Subunit on Endothelial Cells and Induces Vascular Insulin Resistance in Type 2 Diabetes

2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Thaysa Ghiarone Araujo Silva ◽  
Jorge Castorena‐Gonzalez ◽  
Robert M. Restaino ◽  
Christopher A. Foote ◽  
Mariana Morales‐Quinones ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Endothelial Cells ◽  
Insulin Receptor ◽  
Α Subunit
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