β cells keep bad epigenetic memories of palmitate
نویسندگان
چکیده
Palmitic acid, or hexadecanoic acid, a 16-carbon saturated fatty acid (FA), accounts for approximately 38% of the total circulating FA in lean or obese humans. In an article published in BMC Medicine, Hall et al. report that cultured islets from healthy donors, when exposed to palmitate, undergo changes in CpG methylation that are associated with modifications of expression in 290 genes. Their results provide a first look at the mechanisms used by the endocrine pancreas of humans to keep a durable genomic imprint from their exposure to FA that can influence gene expression and possibly cell phenotype in the long term. It is likely that such studies will help understand the epigenetic response of β cells to a disturbed metabolic environment, especially one created by obesity.
منابع مشابه
Impaired cAMP generation contributes to defective glucose-stimulated insulin secretion after long-term exposure to palmitate.
Chronic palmitate exposure impairs glucose-stimulated insulin secretion and other aspects of β-cell function, but the underlying mechanisms are not known. Using various live-cell fluorescence imaging approaches, we show here that long-term palmitate treatment influences cAMP signaling in pancreatic β-cells. Glucose stimulation of mouse and human β-cells induced oscillations of the subplasma-mem...
متن کاملPalmitate induces autophagy in pancreatic β-cells via endoplasmic reticulum stress and its downstream JNK pathway.
Endoplasmic reticulum (ER) stress and autophagy have both been reported to be associated with lipotoxicity in β-cells, yet the relationship between them has not been fully clarified. In the present study, we tested the hypothesis that the ER stress-autophagic pathway in β-cells is a downstream pathway activated following saturated fatty acid treatment. Mouse insulinoma (MIN6) β-cells were treat...
متن کاملBcl-2 maintains the mitochondrial membrane potential, but fails to affect production of reactive oxygen species and endoplasmic reticulum stress, in sodium palmitate-induced β-cell death
BACKGROUND Sodium palmitate causes apoptosis of β-cells, and the anti-apoptotic protein Bcl-2 has been shown to counteract this event. However, the exact mechanisms that underlie palmitate-induced pancreatic β-cell apoptosis and through which pathway Bcl-2 executes the protective effect are still unclear. METHODS A stable Bcl-2-overexpressing RINm5F cell clone (BMG) and its negative control (...
متن کاملA role for aberrant protein palmitoylation in FFA-induced ER stress and β-cell death.
Exposure of insulin-producing cells to elevated levels of the free fatty acid (FFA) palmitate results in the loss of β-cell function and induction of apoptosis. The induction of endoplasmic reticulum (ER) stress is one mechanism proposed to be responsible for the loss of β-cell viability in response to palmitate treatment; however, the pathways responsible for the induction of ER stress by palm...
متن کاملSerotonin- and Dopamine-Related Gene Expression in db/db Mice Islets and in MIN6 β-Cells Treated with Palmitate and Oleate
High circulating nonesterified fatty acids (NEFAs) concentration, often reported in diabetes, leads to impaired glucose-stimulated insulin secretion (GSIS) through not yet well-defined mechanisms. Serotonin and dopamine might contribute to NEFA-dependent β-cell dysfunction, since extracellular signal of these monoamines decreases GSIS. Moreover, palmitate-treated β-cells may enhance the express...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
دوره 12 شماره
صفحات -
تاریخ انتشار 2014