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Free fatty acids regulate gut incretin glucagon-like peptide-1 secretion through GPR120
TLDR
It is shown that a G-protein-coupled receptor, GPR120, which is abundantly expressed in intestine, functions as a receptor for unsaturated long-chain FFAs and promotes the secretion of GLP-1 in vitro and in vivo, and increases circulating insulin.
The gut microbiota suppresses insulin-mediated fat accumulation via the short-chain fatty acid receptor GPR43
TLDR
It is demonstrated that G PR43-deficient mice are obese on a normal diet, whereas mice overexpressing GPR43 specifically in adipose tissue remain lean even when fed a high-fat diet.
Dysfunction of lipid sensor GPR120 leads to obesity in both mouse and human
TLDR
This study demonstrates that the lipid sensor GPR120 has a key role in sensing dietary fat and, therefore, in the control of energy balance in both humans and rodents.
Short-chain fatty acids and ketones directly regulate sympathetic nervous system via G protein-coupled receptor 41 (GPR41)
TLDR
It is established that SCFAs and ketone bodies directly regulate GPR41-mediated SNS activity and thereby control body energy expenditure in maintaining metabolic homeostasis.
Primary systemic carnitine deficiency is caused by mutations in a gene encoding sodium ion-dependent carnitine transporter
TLDR
These mutations provide the first evidence that loss of OCTN2 function causes primary systemic carnitine deficiency, an autosomal recessive disorder characterized by progressive cardiomyopathy, skeletal myopathy, hypoglycaemia and hyperammonaemia.
Free fatty acids induce cholecystokinin secretion through GPR120
TLDR
Results indicate that long-chain FFAs induce CCK secretion through GPR120-coupled Ca2+signaling, which was specifically inhibited by transfection of GPR 120-specific, but not GPR40- specific, short hairpin RNA.
Identification of novel microRNA targets based on microRNA signatures in bladder cancer
TLDR
The target search algorithm and gene‐expression profiling in BCs revealed that Keratin7 (KRT7) mRNA was a common target of the downregulated miRNAs, and the mRNA expression levels of KRT7 were significantly higher inBCs than in NBEs.
Mice Genetically Deficient in Vasopressin V1a and V1b Receptors Are Resistant to Jet Lag
TLDR
Pharmacological blockade of V1a and V1b in the SCN of wild-type mice resulted in accelerated recovery from jet lag, which highlights the potential of vasopressin signaling as a therapeutic target for management of circadian rhythm misalignment, such as jet lag and shift work.
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