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Circulating Epigenetic Signatures Classifying Brain Insulin Resistance in humans

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE301739 | GEO | 2026/04/08

REPOSITORIES: GEO

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Circulating Epigenetic Signatures Classifying Brain Insulin Resistance in humans [1]

Project description:Brain insulin action plays an important role in metabolic and cognitive health but so far, there is no biomarker available to assess brain insulin resistance in humans. Here, we developed a machine learning framework based on blood DNA methylation profiles of participants who did not have Type 2 Diabetes with and without brain insulin resistance and detailed metabolic phenotyping.

2026-04-08 | GSE301735 | GEO

Circulating Epigenetic Signatures Classifying Brain Insulin Resistance in humans [2]

2026-04-08 | GSE301736 | GEO

Circulating Epigenetic Signatures Classifying Brain Insulin Resistance in humans

Project description:Circulating Epigenetic Signatures Classifying Brain Insulin Resistance in humans

| PRJNA1287498 | ENA

Circulating Epigenetic Signatures Classifying Brain Insulin Resistance in humans [1]

Project description:Circulating Epigenetic Signatures Classifying Brain Insulin Resistance in humans [1]

| PRJNA1287497 | ENA

Circulating Epigenetic Signatures Classifying Brain Insulin Resistance in humans [2]

Project description:Circulating Epigenetic Signatures Classifying Brain Insulin Resistance in humans [2]

| PRJNA1287500 | ENA

Skeletal muscle and plasma lipidomic signatures of insulin resistance and overweight/obesity in humans.

Project description:ObjectiveAlterations in lipids in muscle and plasma have been documented in insulin-resistant people with obesity. Whether these lipid alterations are a reflection of insulin resistance or obesity remains unclear.MethodsNondiabetic sedentary individuals not treated with lipid-lowering medications were studied (n = 51). Subjects with body mass index (BMI) > 25 kg/m(2) (n = 28) were stratified based on median glucose infusion rate during a hyperinsulinemic-euglycemic clamp into insulin-sensitive and insulin-resistant groups (above and below median, obesity/insulin-sensitive and obesity/insulin-resistant, respectively). Lean individuals (n = 23) served as a reference group. Lipidomics was performed in muscle and plasma by liquid chromatography electrospray ionization-tandem mass spectrometry. Pathway analysis of gene array in muscle was performed in a subset (n = 35).ResultsIn muscle, insulin resistance was characterized by higher levels of C18:0 sphingolipids, while in plasma, higher levels of diacylglycerol and cholesterol ester, and lower levels of lysophosphatidylcholine and lysoalkylphosphatidylcholine, indicated insulin resistance, irrespective of overweight/obesity. The sphingolipid metabolism gene pathway was upregulated in muscle in insulin resistance independent of obesity. An overweight/obesity lipidomic signature was only apparent in plasma, predominated by higher triacylglycerol and lower plasmalogen species.ConclusionsMuscle C18:0 sphingolipids may play a role in insulin resistance independent of excess adiposity.

| S-EPMC6585800 | biostudies-literature

Towards epigenetic understanding and therapy of insulin resistance by intranuclear insulin [DNA methylation]

Project description:There is evidence indicating the involvement of DNA methylation memory in maintaining gene expression patterns associated with insulin resistance. Although the exact mechanism remains unknown, it has been proved that insulin resistance is correlated to low heat shock protein (HSP) expression. We reveal that intranuclear insulin can reduce HSP DNA methylation level to up-regulate HSP protein expression and result in long term cure of hyperglycemia.

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The epigenetic signature of systemic insulin resistance in obese women

Project description:This SuperSeries is composed of the SubSeries listed below.

2016-08-01 | GSE76399 | GEO

The epigenetic signature of systemic insulin resistance in obese women [BL]

Project description:Impaired ability of insulin to stimulate cellular glucose uptake and regulate metabolism, that is insulin resistance (IR), links adiposity to metabolic disorders such as type 2 diabetes (T2D), dyslipidemia and cardiovascular disease (Langenberg, 2012). Both genetic and epigenetic factors are implicated in development of systemic IR (Vaag, 2001). IR is characterized by elevated levels of fasting insulin in the general circulation. The aim of this study is to explore whether white adipose tissue (WAT) epigenetic dysregulation is associated with systemic IR by global CpG methylation and gene expression profiling in subcutaneous and visceral adipose tissue. A secondary aim is to determine whether the DNA methylation signature in peripheral blood mononuclear cells reflect WAT methylation, and can be used as marker for systemic IR.

2016-08-01 | GSE76285 | GEO

The epigenetic signature of systemic insulin resistance in obese women [SC]

2016-08-01 | GSE76398 | GEO