β Cell-specific deletion of guanylyl cyclase A, the receptor for atrial natriuretic peptide, accelerates obesity-induced glucose intolerance in mice.
Sabine TauscherHitoshi NakagawaKatharina VölkerFranziska WernerLisa KrebesTamara PotapenkoSören DooseAndreas L BirkenfeldHideo A BabaMichaela KuhnPublished in: Cardiovascular diabetology (2018)
Our studies of β GC-A KO mice demonstrate that the cardiac hormones ANP and BNP do not modulate β-cell's growth and secretory functions under physiological, normal dietary conditions. However, endogenous NP/GC-A signaling improves the initial adaptative response of β-cells to HFD-induced obesity. Impaired β-cell NP/GC-A signaling in obese individuals might contribute to the development of type 2 diabetes.
Keyphrases
- high fat diet induced
- metabolic syndrome
- weight loss
- single cell
- cell therapy
- insulin resistance
- type diabetes
- high glucose
- adipose tissue
- high fat diet
- heart failure
- stem cells
- bariatric surgery
- physical activity
- gas chromatography
- oxidative stress
- mesenchymal stem cells
- endothelial cells
- drug induced
- left atrial
- high resolution
- binding protein