In Drosophila, the roles of components of the adipokinetic hormone signaling pathway (adipokinetic hormone, Akh, or its receptor, AkhR) in the response to a chronic high-sugar diet have been investigated.
In insects, adipokinetic hormone (AKH) appears to be functionally analogous to mammalian glucagon, however, some aspects differ. In mammals, glucagon increases glycemia by promoting catabolism of both fat and glycogen. In Drosophila, adipokinetic hormone (AKH) regulates catabolism of lipids analogously to mammalian glucagon, but AKH does not appear to induce catabolism of glycogen (under normal dietary conditions).
A chronic high-sugar diet results in hyperglycemia in Drosophila; this response requires Akh signaling in the fat body. However, acute high-sugar feeding does not elicit the same response. Thus, there appears to be a pathogenic, but not a normal physiological, enhancement of AKH response in the fly fat body under a chronic high-sugar diet. The Akh response observed in the fly fat body has been shown to be regulated by production of activin-β (Actβ) by a subset of midgut cells.
[updated Feb. 2019 by FlyBase; FBrf0222196]
In mammals, glucagon increases glycemia by promoting catabolism of both fat and glycogen. In the fly, adipokinetic hormone (AKH) regulates catabolism of lipids analogously to mammalian glucagon, but AKH does not induce catabolism of glycogen (Galikova and Klepsatel, 2018, and references cited therein; pubmed:29954158; FBrf0239311).
Dmel\Akh is postulated to play a role analogous to some of the functions of mammalian glucagon.
Moderate-scoring ortholog of human gonadotropin releasing hormone receptor (GNRHR); multiple lower-scoring orthologs in both species. Dmel\AkhR shares 32% identity and 56% similarity with the human GNRHR gene. Dmel\AkhR is less closely related to the human glucagon receptor (GCGR), sharing 25% identity and 41% similarity.
