Advances in Metabolic Disorders, Volume 3 is a compendium of papers that discusses the regulation of ketogenesis, spontaneous diabetes, ethanol-induced hypoglycemia, and hormonal syndromes associated with neoplasia. One paper discusses the primary role of long-chain fatty acids in synergistically controlling enhanced ketogenesis and gluconeogenesis found in the liver at the cellular level. Another paper notes that in rodent experiments, when hypertrophy and hyperplasia are maintained without exhaustion or degeneration and are sufficient in degree, a new equilibrium emerges leading to near-normalization or compensated diabetes. The opposite occurs when hypertrophy and hyperplasia are limited in degree or in duration: decompensation occurs, diabetes progresses. Some papers describe metabolic disorders of the ovary, erythropoietin, and thyroid diseases. One paper analyzes the pathological conditions arising from impairments of the hypothalamic-pituitary-ovarian-uterine axis that can cause disturbances in normal reproduction Another paper investigates if a competitive relationship exists between thyrotropin (TSH) and long-acting thyroid stimulator (LATS). In vivo and in vitro studies show that the effect of LATS are associated mainly with a delayed onset of action. Biochemists, micro-biologists, endocrinologists, and researchers dealing with microchemistry, bacteriology and immunology will find this collection valuable.

Advances in Metabolic Disorders, Volume 3 is a compendium of papers that discusses the regulation of ketogenesis, spontaneous diabetes, ethanol-induced hypoglycemia, and hormonal syndromes associated with neoplasia. One paper discusses the primary role of long-chain fatty acids in synergistically controlling enhanced ketogenesis and gluconeogenesis found in the liver at the cellular level. Another paper notes that in rodent experiments, when hypertrophy and hyperplasia are maintained without exhaustion or degeneration and are sufficient in degree, a new equilibrium emerges leading to near-normalization or compensated diabetes. The opposite occurs when hypertrophy and hyperplasia are limited in degree or in duration: decompensation occurs, diabetes progresses. Some papers describe metabolic disorders of the ovary, erythropoietin, and thyroid diseases. One paper analyzes the pathological conditions arising from impairments of the hypothalamic-pituitary-ovarian-uterine axis that can cause disturbances in normal reproduction Another paper investigates if a competitive relationship exists between thyrotropin (TSH) and long-acting thyroid stimulator (LATS). In vivo and in vitro studies show that the effect of LATS are associated mainly with a delayed onset of action. Biochemists, micro-biologists, endocrinologists, and researchers dealing with microchemistry, bacteriology and immunology will find this collection valuable.