scholarly journals Integratome analysis of adipose tissues reveals abnormal epigenetic regulation of adipogenesis, inflammation, and insulin signaling in obese individuals with type 2 diabetes

2021 ◽  
Vol 11 (12) ◽  
Author(s):  
Nana Jin ◽  
Heung‐Man Lee ◽  
Yong Hou ◽  
Allen C.S. Yu ◽  
Jing‐Woei Li ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Epigenetic Regulation ◽  
Insulin Signaling ◽  
Adipose Tissues

scholarly journals Insulin Resistance and Diabetes Mellitus in Alzheimer’s Disease

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1236
Author(s):  
Jesús Burillo ◽  
Patricia Marqués ◽  
Beatriz Jiménez ◽  
Carlos González-Blanco ◽  
Manuel Benito ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Alzheimer’S Disease ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Alzheimer's Disease ◽  
Type 2 Diabetes Mellitus ◽  
Insulin Signaling ◽  
Molecular Mechanisms ◽  
Progressive Disease

Type 2 diabetes mellitus is a progressive disease that is characterized by the appearance of insulin resistance. The term insulin resistance is very wide and could affect different proteins involved in insulin signaling, as well as other mechanisms. In this review, we have analyzed the main molecular mechanisms that could be involved in the connection between type 2 diabetes and neurodegeneration, in general, and more specifically with the appearance of Alzheimer’s disease. We have studied, in more detail, the different processes involved, such as inflammation, endoplasmic reticulum stress, autophagy, and mitochondrial dysfunction.

scholarly journals Metabolic inflexibility of white and brown adipose tissues in abnormal fatty acid partitioning of type 2 diabetes

2012 ◽  
Vol 2 (S2) ◽  
pp. S37-S42 ◽  
Author(s):  
T Grenier-Larouche ◽  
S M Labbé ◽  
C Noll ◽  
D Richard ◽  
A C Carpentier
Keyword(s):  
Type 2 Diabetes ◽  
Fatty Acid ◽  
Adipose Tissues ◽  
Brown Adipose ◽  
Metabolic Inflexibility

Comprehensive Review on Neuro-Degenerative Type 3DM

2021 ◽  
Vol 18 ◽  
Author(s):  
Chandani V. Chandarana ◽  
Salona Roy
Keyword(s):  
Type 2 Diabetes ◽  
Insulin Signaling ◽  
Insulin Signalling ◽  
Amyloid Β ◽  
Diabetes Mellitus Type 1 ◽  
Current Data ◽  
The Body ◽  
Type I ◽  
Therapeutic Benefits

: Alzheimer disease (AD) is thought to be the metabolic illness raised by defective insulin signaling, insulin resistance, and low insulin levels in the brain, according to a growing body of research. The "Type 3 diabetes" has been postulated for AD because reduced insulin signalling has molecular and physiological consequences that are comparable to Type I and Type 2 diabetes mellitus (Type 1 DM and Type 2 DM, respectively). The similarities between type 2 diabetes and Alzheimer's disease suggest that these clinical trials might yield therapeutic benefits. However, it's important to note that lowering your risk of Alzheimer's dementia, whether you have diabetes or not, is still a multidimensional process involving factors like exercise, smoking, alcohol, food, and mental challenge. The current aim is to show the relationship between T3D and AD being based on both the processing of amyloid-β (Aβ) precursor protein toxicity and the clearance of Aβ are the result of an impaired insulin signaling. The brain's metabolism with its high lipid content and energy needs, places excess demands on mitochondria and appears more susceptible to oxidative damage than the rest of the body. Current data suggests that increased oxidative stress relates to amyloid-β (Aβ) pathology and onset of AD.

scholarly journals Phenylalanine Impairs Insulin Signaling and Inhibits Glucose Uptake by Modifying IRβ

2021 ◽  
Author(s):  
Qian Zhou ◽  
Wan-Wan Sun ◽  
Jia-Cong Chen ◽  
Huilu Zhang ◽  
Jie Liu ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Amino Acids ◽  
Insulin Receptor ◽  
Glucose Uptake ◽  
Insulin Signaling ◽  
Trna Synthetase ◽  
Blood Samples ◽  
Receptor Beta

Abstract Although elevated circulating amino acids are associated with the onset of type 2 diabetes (T2D), how amino acids act on cell insulin signaling and glucose uptake remains unclear. Herein, we report that phenylalanine modifies insulin receptor beta (IRβ) and inactivates insulin signaling and glucose uptake. Mice fed phenylalanine-rich chow or overexpressing human phenylalanyl-tRNA synthetase (hFARS) developed insulin resistance and symptoms of T2D. Mechanistically, FARS phenylalanylated lysine 1057/1079 of IRβ (F-K1057/1079) inactivated IRβ and prevented insulin from generating insulin signaling to promote glucose uptake by cells. SIRT1 reversed F-K1057/1079 and counteracted the insulin-inactivating effects of hFARS and phenylalanine. F-K1057/1079 and SIRT1 levels of white cells of T2D patients’ blood samples were positively and negatively correlated with T2D onset, respectively. Blocking F-K1057/1079 with phenylalaninol sensitized insulin signaling and relieved T2D symptoms in hFARS-transgenic and db/db mice. We revealed mechanisms of how phenylalanylation inactivates insulin signaling that may be employed to control T2D.

scholarly journals A Transcriptomic and Proteomic Atlas of Obesity and Type 2 Diabetes in Cynomolgus Monkeys

2021 ◽  
Author(s):  
Xianglong Zhang ◽  
Ying Lei ◽  
Oliver Homann ◽  
Marina Stolina ◽  
Songli Wang ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Immune Response ◽  
Nonhuman Primate ◽  
Metabolic Disorders ◽  
Healthy Controls ◽  
Adipose Tissues ◽  
Cynomolgus Monkeys ◽  
Single Cell Rna Sequencing

Obesity and type 2 diabetes (T2D) remain major global healthcare challenges and developing therapeutics necessitate using nonhuman primate models. Here, we present transcriptomic and proteomic analyses of all the major organs of cynomolgus monkeys with spontaneous obesity or T2D in comparison to healthy controls. Molecular changes occur predominantly in the adipose tissues of individuals with obesity, while extensive expression perturbations among T2D individuals are observed in many tissues, such as the liver, kidney, brain, and heart. Immune response-related pathways are upregulated in obesity and T2D, whereas metabolism and mitochondrial pathways are downregulated. Incorporating human single-cell RNA sequencing findings corroborates the role of macrophages and monocytes in obesity. Moreover, we highlight some potential therapeutic targets including SLC2A1 and PCSK1 in obesity as well as SLC30A8 and SLC2A2 in T2D. Our findings provide insights into tissue-specific molecular foundations of obesity and T2D and reveal the mechanistic links between these two metabolic disorders.

Genistein and Momordica charantia L. prevents oxidative stress and upregulate proglucagon and insulin receptor mRNA in diabetic rats.

2021 ◽  
Author(s):  
Wusa Makena ◽  
Abdullahi Ibrahim Iliya ◽  
Joseph Olajide Hambolu ◽  
James Abrak Timbuak ◽  
Uduak Emmanuel Umana ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Type 2 Diabetes ◽  
Insulin Receptor ◽  
Mrna Expression ◽  
Insulin Signaling ◽  
Diabetic Rats ◽  
Momordica Charantia ◽  
Receptor Mrna ◽  
Group I

Type 2 diabetes (T2D) occur as a result of insulin resistance and malfunction in insulin signaling. Controlling hyperglycemia and activation of insulin signaling are important in the management of T2D. The study aimed to evaluate the effect of Genistein and Momordica charantia L. fruit on oxidative stress, markers of inflammation, and their role on proglucagon and insulin receptor mRNA expression by RT-PCR in diabetic rats. Thirty-five albino rats were divided into seven groups (n=5). Group I (non-diabetic) and group II (diabetic control) were treated with distilled water, groups III and IV received 250mg/kg and 500mg/kg lyophilized MCF respectively. Groups V and VI received 10mg/kg and 20mg/kg Genistein respectively while group VII received 500mg/kg Metformin. The administration lasted for 28 days. MCF and Genistein significantly reduced IL-1β and TNFα levels that was elevated in serum of diabetic rats. Treatment with MCF and Genistein significant increased the expression of proglucagon mRNA in the small intestine and insulin receptor mRNA in the liver of diabetic rats. In conclusion, MCF and Genistein ameliorate type 2 diabetes complications by preventing the loss of insulin-positive cells, inhibiting IL-1β and TNFα and up-regulating proglucagon and insulin receptor mRNA expression. Novelty: • MCF and Genistein has an inhibitory effect on diabetic induced IL-1β and TNFα production. • MCF and Genistein up-regulates proglucagon and insulin receptor mRNA expression.

scholarly journals Reconstruction of Protein-Protein Interaction Network of Insulin Signaling inHomo Sapiens

2010 ◽  
Vol 2010 ◽  
pp. 1-7 ◽  
Author(s):  
Saliha Durmuş Tekir ◽  
Pelin Ümit ◽  
Aysun Eren Toku ◽  
Kutlu Ö. Ülgen
Keyword(s):  
Type 2 Diabetes ◽  
Insulin Signaling ◽  
Homo Sapiens ◽  
Interaction Network ◽  
Protein Protein Interaction ◽  
Signaling Mechanisms ◽  
Reconstructed Network ◽  
Protein Protein Interaction Network

Diabetes is one of the most prevalent diseases in the world. Type 1 diabetes is characterized by the failure of synthesizing and secreting of insulin because of destroyed pancreaticβ-cells. Type 2 diabetes, on the other hand, is described by the decreased synthesis and secretion of insulin because of the defect in pancreaticβ-cells as well as by the failure of responding to insulin because of malfunctioning of insulin signaling. In order to understand the signaling mechanisms of responding to insulin, it is necessary to identify all components in the insulin signaling network. Here, an interaction network consisting of proteins that have statistically high probability of being biologically related to insulin signaling inHomo sapienswas reconstructed by integrating Gene Ontology (GO) annotations and interactome data. Furthermore, within this reconstructed network, interacting proteins which mediate the signal from insulin hormone to glucose transportation were identified using linear paths. The identification of key components functioning in insulin action on glucose metabolism is crucial for the efforts of preventing and treating type 2 diabetes mellitus.

Insulin Signaling and Action in Fat Cells: Associations with Insulin Resistance and Type 2 Diabetes

1999 ◽  
Vol 892 (1 THE METABOLIC) ◽  
pp. 119-126 ◽  
Author(s):  
ULF SMITH ◽  
METTE AXELSEN ◽  
EUGENIA CARVALHO ◽  
BJORN ELIASSON ◽  
PER-ANDERS JANSSON ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Insulin Signaling ◽  
Fat Cells
Sign in / Sign up

Export Citation Format

Share Document