Endocrinology · 1960 · 141 citations · 0 references
Life SciencesBiochemistryEndocrinologyHormone BiochemistryMetabolismReproductive EndocrinologyAdrenal HormonesAdrenal Steroid HormonesEndocrine BiochemistryEndocrine PhysiologyHormonal Control Of MetabolismHormone MetabolismAdrenal Cortex FunctionAdrenal Cortex PhysiologyAdrenal Hormone BiochemistryCyclic Adenosine Monophosphate PathwayEndocrine HormonesEndocrine Regulation Of MetabolismHormone Metabolic RegulationOxidation
The authors discuss why ACTH does not inhibit glucose oxidation, citing Haynes’ work, and note that the hexose monophosphate pathway generates TPNH, a cofactor that may regulate hormone production. They examined glucose‑1‑C14 and glucose‑6‑C14 oxidation pathways in vitro using adrenal, ovary, testis, pituitary, and parathyroid tissue slices. Their results show an active hexose monophosphate pathway in all endocrine glands studied, with TSH stimulating thyroid glucose oxidation but no effect from FSH, LH, hCG, or anterior pituitary powder, and ACTH or cAMP failing to inhibit adrenal cortex oxidation, implying TPNH may influence hormone regulation.
Pathways of glucose oxidation using glucose-1-C14 and glucose-6-C14 have been studied in vitro in adrenal, ovary, testis, pituitary and parathyroid slices. The results indicate the existence of an active hexose monophosphate pathway in all endocrine glands studied. Although in similar experiments TSH in vitro was capable of stimulating glucose oxidation in thyroid (1), no effects of FSH, LH, chorionic gonadotrophin or anterior pituitary powder were observed in ovary or testis. Neither ACTH nor 3′5′ cyclic adenosine monophosphate inhibited glucose oxidation in slices of adrenal cortex. Possible causes for this absence of inhibition are discussed in light of the recent work by Haynes on the mechanism of action of ACTH (6). The hexose monophosphatc pathway for glucose metabolism in endocrine tissue is a source of TPNH, and this cofactor may be of importance in the regulation of hormone production.