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It is suggested that SEM and EXE exert complementary effects on glycemic and lipid metabolism, with partially distinct metabolic outcomes that may involve different underlying mechanisms.
Preliminary findings indicate that semaglutide integrates bioenergetic and Ca2⁺-signaling responses in beta cells through combined modulation of mitochondrial remodeling, respiratory activity, and organelle-dependent Ca2⁺ handling.
Astrocyte-specific mitochondrial dysfunctions and calcium dysregulation are identified as key features of LRRK2- and PRKN-related pathology, providing new insights into how glial metabolic alterations contribute to neurodegeneration in PD.
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