Adrenomedullin, a hormone first identified in an adrenal medullary tumor, disrupts the effect of insulin on the endothelium of blood vessels, leading to insulin resistance linked to obesity and type 2 diabetes. The clue to this discovery lies in a molecular pathway that could be blocked to restore insulin function.
Ulcerative colitis is a chronic, immune-mediated disorder of the colon and rectum characterized by mucosal inflammation that damages the bowel wall surface. Current therapeutic options include 5-aminosalicylates, corticosteroids or anti-TNF agents, but there is a need for new strategies to obtain higher remission rates and less systemic immunosuppression.
Death receptor 3 (DR3) is the only signaling receptor for TNF superfamily ligand TL1A, the dysregulation of which has been implicated in multiple inflammatory diseases such as inflammatory bowel disease (IBD). Blockade of TL1A has been shown to induce significant clinical responses in IBD.
Acute pancreatitis (AP) is a gastrointestinal disorder characterized by inflammation and necrosis of the pancreatic acinar cells. Mitochondrial homeostasis is key to energy metabolism and redox homeostasis, both of which are essential for pancreatic functioning, where oxidative phosphorylation (OXPHOS) plays a crucial role.
Researchers from Ocean University of China and Qingdao Marine Science and Technology Center published data from a preclinical study that investigated the impact of the quinazolinone derivative MR-2938 on gut microbiota during colitis. A dextran sodium sulfate (DSS)-induced colitis mouse model was constructed, and the animals were treated with MR-2938 (50 or 100 mg/kg).
Understanding the mechanisms of resistance to cancer treatments is necessary to find effective therapies at different stages of the disease. Scientists at UT Southwestern Medical Center studied the most frequent mutation in pancreatic ductal adenocarcinoma (PDAC), identified an escape route to a therapy in clinical trials, blocked it with another experimental compound and reduced tumors in mice.
It was hypothesized that the crosstalk between Toll-like receptors, especially Toll-like receptor 4 (TLR4), and serotonergic machinery during inflammation may be an important factor for understanding the neuroimmune mechanisms participating in inflammatory bowel disease pathogenesis.
Hypoxia-inducible factors (HIFs) are crucial to maintain oxygen homeostasis by regulating cellular metabolic adaptation under hypoxia conditions. Depletion of factor inhibiting HIF (FIH), an enzyme that negatively regulates the activity of the HIF-1α isoform, has been associated with reductions in hepatic steatosis and body mass in mice.
Fatty acid synthase (FASN), an enzyme that drives de novo lipogenesis, plays a relevant role in metabolic disorders such as obesity, non-alcoholic fatty liver disease (NAFLD) or type 2 diabetes. Denifanstat (TVB-2640), a FASN inhibitor, has recently shown positive results in a phase II study in patients with metabolic dysfunction-associated steatohepatitis (MASH).
The liver and pancreas are the main actors in glucose metabolism, but not the only ones. Muscles, adipose tissue and the brain play different roles. However, the prize for the best new actor in glucagon production goes to the innate lymphoid cells (ILCs), which, according to a study published in Science, respond to intestine neuron signals traveling to the pancreas to control glucose.
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