Dysglycemia Shapes Visceral Adipose Tissue's Response to GIP, GLP-1 and Glucagon in Individuals with Obesity.

Visceral adipose tissue (VAT) metabolic fingerprints differ according to body mass index (BMI) and glycemic status. Glucagon-like peptide 1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP) and glucagon are gut-associated hormones that play an important role in regulating energy and glucose homeostasis, although their metabolic actions in VAT are still poorly characterized. Our aim was to assess whether GLP-1, GIP and glucagon influence the VAT metabolite profile.

α-Tubulin detyrosination links the suppression of MCAK activity with taxol cytotoxicity.

α/β-Tubulin posttranslational modifications (PTMs) generate microtubule diversity, but whether they account for cancer cell resistance to microtubule-targeting drugs remains unknown. Here, we performed a pilot dissection of the "cancer tubulin code" using the NCI-60 cancer cell panel. We found that acetylated, detyrosinated, and ∆2-α-tubulin that typically accumulate on stable microtubules were uncoupled in many cancer cells.

Adipose Tissue Epigenetic Profile in Obesity-Related Dysglycemia - A Systematic Review.

Background: Obesity is a major risk factor for dysglycemic disorders, including type 2 diabetes (T2D). However, there is wide phenotypic variation in metabolic profiles. Tissue-specific epigenetic modifications could be partially accountable for the observed phenotypic variability.

Visceral Adipose Tissue Displays Unique Metabolomic Fingerprints in Obesity, Pre-Diabetes and Type 2 Diabetes.

Visceral adipose tissue (VAT) metabolic profiling harbors the potential to disentangle molecular changes underlying obesity-related dysglycemia. In this study, the VAT exometabolome of subjects with obesity and different glycemic statuses are analyzed. The subjects ( = 19) are divided into groups according to body mass index and glycemic status: subjects with obesity and euglycemia (Ob+NGT, = 5), subjects with obesity and pre-diabetes (Ob+Pre-T2D, = 5), subjects with obesity and type 2 diabetes under metformin treatment (Ob+T2D, = 5) and subjects without obesity and with euglycemia (Non-Ob, = 4), used as controls.