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. 2013 Mar 14;62(4):1152–1158. doi: 10.2337/db12-0228

FIG. 4.

FIG. 4.

The glucoregulatory action of proline requires flux through astrocytic LDH-A in the MBH. A: Time line for studies on the effect of lentiviral shRNA-mediated LDH-A knockdown and pancreatic insulin clamps. B: Schematic of pancreatic clamp procedure in rats receiving central (MBH) infusions of proline. C: Representative Western blot of LDH-A knockdown in the MBH of rats. D: Quantification of LDH-A expression in the MBH of rats receiving intrahypothalamic injections of either a control shRNA lentivirus (n = 6, white bar) or LDH-A shRNA lentivirus (n = 6, black bar). E–H: Effect of central vehicle (VEH) and proline (PRO) in animals injected in the MBH with either control nonsilencing (n = 6, white bars) or LDH-A shRNA (n = 6, black bars) on glucose infusion rate (E), glucose production (F), suppression of glucose production (G), and glucose utilization (H). I: Schematic of the proposed mechanism for the regulation of liver glucose fluxes by proline by the ANLS in the hypothalamus. Astrocytes express MCT4 and LDH-A, whereas neurons are enriched in MCT2 and LDH-B. *P < 0.05 vs. control. All values are mean ± SEM. α-KG, α-ketoglutarate; ARC, arcuate nucleus of the hypothalamus; CON, control; DHAP, dihydroxyacetone phosphate; DMX, dorsal motor nucleus of the vagus; Glu, glutamate; KATP, ATP-sensitive potassium channel; NTS, nucleus of the solitary tract; PEP, phosphoenolpyruvate; SUR, sulfonylurea receptor; TCA, tricarboxylic acid cycle.