Regulatory Roles of MicroRNAs in Diabetes

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Annotation Summary

Term Occurence Count Dictionary
hyperinsulinemia 1 endocrinologydiseases
maturity-onset diabetes of the young 1 endocrinologydiseases
obesity 3 endocrinologydiseases
Insulin 7 endocrinologydiseasesdrugs
diabetes mellitus 6 endocrinologydiseases
hyperglycemia 2 endocrinologydiseases

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Select Drug Character Offset Drug Term Instance
Insulin 9364 pancreatic β-cell functions, and the dysregulation of miRNAs may lead to diabetes mellitus.3. miRNAs and Insulin Resistance (IR)IR refers to the impaired cellular response to insulin and the inability of normal amounts
Insulin 10137 associated with defects in insulin signaling. Notably, miRNAs may link insulin signaling and IR.3.1. Insulin Receptor (INSR)The ligand-receptor interaction is the first step of insulin signaling. Mice lacking
Insulin 10802 the 3′-UTR of INSR, resulting in impairment of insulin signaling in hepatocytes [[39],[40]].3.2. Insulin Receptor Substrate 1/2 (IRS-1/2)Insulin receptor substrate 1 (IRS-1) serves as the key molecule in the
Insulin 10842 impairment of insulin signaling in hepatocytes [[39],[40]].3.2. Insulin Receptor Substrate 1/2 (IRS-1/2) Insulin receptor substrate 1 (IRS-1) serves as the key molecule in the insulin signaling pathway in peripheral
Insulin 12418 IRS-1. Thus, enhanced miR-103/107 levels are concomitant with a decreased stability of IRS-1 [[45]]. Insulin receptor substrate 2 (IRS-2) is the alternative substrate of the INSR in IRS-1-deficient conditions.
Insulin 23687 progenitor cellshuman[[26]]miR-9-human fetal isletshuman[[27]]miR-376-human fetal isletshuman[[27]] Insulin secretionmiR-375MtpnMIN-6 cellsmouse[[28]]miR-184Ago 2MIN-6 cellsmouse[[29]]miR-7a-β-cells of diabetic
Insulin 25185 obesity micemouse[[45]]miR-802Hnf1βHepa1-6 cellsmouse[[58]]miR-106bMfn2C2C12 cellsmouse[[59]]IR— Insulin resistance; miR-378/378 *—miR-378 and miR-378 * are two mature microRNAs originate from opposite arms
Select Disease Character Offset Disease Term Instance
diabetes mellitus 833 biological and pathological processes. Disruption of miRNA levels correlates with many diseases, including diabetes mellitus , a complex multifactorial metabolic disorder affecting >400 million people worldwide. miRNAs are involved
diabetes mellitus 980 metabolic disorder affecting >400 million people worldwide. miRNAs are involved in the pathogenesis of diabetes mellitus by affecting pancreatic β-cell functions, insulin resistance, or both. In this review, we summarize
diabetes mellitus 1248 important miRNAs in diabetes, as well as the potential of circulating miRNAs as diagnostic markers for diabetes mellitus .1. MicroRNAs (miRNAs) and DiabetesDiabetes mellitus is a progressive metabolic disease that is characterized
diabetes mellitus 1917 diagnosed with diabetes, T1DM accounts for 5%–10% with the other ~90% having T2DM. T1DM is a form of diabetes mellitus in which not enough insulin is produced by islet cells in the pancreas and subsequently results in high
diabetes mellitus 3192 pathological processes.Since the discovery of miRNAs, an increasing number of them have been found involved in diabetes mellitus pathogenesis [[7]]. Dysregulation of miRNA can lead to profound impairment of glucose metabolism [[8]].
diabetes mellitus 9332 complex regulatory network in pancreatic β-cell functions, and the dysregulation of miRNAs may lead to diabetes mellitus .3. miRNAs and Insulin Resistance (IR)IR refers to the impaired cellular response to insulin and the
hyperglycemia 3425 expression profiles of various tissues (e.g., pancreas, adipose tissue, and liver) from T2DM patients or hyperglycemia animal models have been established in recent years and make it easier to uncover novel miRNA regulators
hyperglycemia 10271 ligand-receptor interaction is the first step of insulin signaling. Mice lacking the INSR gene suffer from hyperglycemia and hyperinsulinemia, and a large number of studies reveal a decrease in INSR in T2DM patients [[38]].
hyperinsulinemia 10289 interaction is the first step of insulin signaling. Mice lacking the INSR gene suffer from hyperglycemia and hyperinsulinemia , and a large number of studies reveal a decrease in INSR in T2DM patients [[38]]. These findings support
maturity-onset diabetes of the young 6181 genetic fatty db/db mice, and inhibits β-cell proliferation and insulin secretion by binding to two maturity-onset diabetes of the young genes, Hnf1α and Neurod1. Meanwhile, the expression of miR-24 increased from 2.0- to 3.5-fold in 8-
obesity 11838 impairs insulin signaling through targeting the 3′-UTR of IRS-1 [[43]]. In maternal diet-induced obesity of offspring and IR in later life, miR-126 plays a negative role via targeting IRS-1 [[44]].Aside from
obesity 12111 indirectly inhibits the expression of IRS-1. For example, in livers and adipose tissues of diet-induced obesity mice, overexpression of miR-103/107 negatively regulates insulin signaling by targeting Cav-1, a caveolae
obesity 25086 cellshuman[[57]]miR-29PparδC2C12 cellsmouse[[53]]miR-103/107Cav-1livers and adipose tissues of diet induced obesity micemouse[[45]]miR-802Hnf1βHepa1-6 cellsmouse[[58]]miR-106bMfn2C2C12 cellsmouse[[59]]IR—Insulin resistance;

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