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Although the exact mechanisms by which the coordinated actions of GLP-1 receptor agonism and NMDA receptor antagonism correct metabolic diseases await further elucidation, the extensive alterations in transcriptomic and proteomic responses within the hypothalamus, linked to glutamatergic signalling and synaptic plasticity, imply that the conjugate might elicit neurostructural changes in GLP-1-receptor-expressing neurons
We see it as a deeper breakdown in communication between the immune system, nutrient absorption, and gut
& Woolhouse, M
On the other hand, prolonged (16 h) stimulation with GLP-1 was shown to promote Hypoxia-Inducible Factor 1 (HIF-1) activity via induction of the mammalian Target of Rapamycin (mTOR) 16
Indeed, a mouse model of impaired (gene knockout) BCAA catabolism showed that accumulation of BCAAs or their intermediate metabolites (branched-chain -keto acids, BCKAs) in the heart suppressed glucose metabolism by decreasing glucose uptake and mitochondrial pyruvate utilization, a key step of glucose oxidation, and promoted fatty acid oxidation 72,74,75
