By using a modified method of Falck, the distribution of nerves containing catecholamines in brown and white fat was studied. The brown fat cells had sympathetic nerve fibers with synaptic varicosities running between all cells. White fat had no sympathetic innervation of the parenchymal cells. Both tissues contained a dense network of fibers around the arterial blood vessels.
With the Falck fluorescent histochemical method for catecholamines, the development of sympathetic nerve fibers in the brown fat of the rat was studied. At birth a low level of catecholamine fluorescence was found in preterminal axon bundles, which have been called here sheathed axons. The fluorescence in these bundles reached a maximum at about 5 days of age. Parenchymal nerve catecholamine fluorescence was discernible at 2 to 3 days of age. These nerves progressively got brighter until adult levels had been reached at about 10–15 days. The sympathetic nerve fiber network seen on arterial blood vessels in the adult was not seen in the young rat until 8–10 days of age. These blood vessel nerves reached maturity at about 15–21 days. The parenchymal nerve innervation was shown to originate in the sympathetic chain. The sympathetic chain gave off sheathed axon bundles which reach the parenchyma by passing along septa or beside blood vessels.
The family of the mammalian GLUT transporters involved in transmembrane translocation of hexoses and related solutes and identified human diseases associated with their malfunction are outlined. The SGLT family of electrogenic transporters and the monocarboxylate and fatty acid transporters are also presented. Classified transport activities of the various amino acid-transporting systems found in the plasma membrane of mammalian cells and cDNAs that encode the proteins mediating this activity are summarized. The transport pathways for water are discussed and the mammalian vitamin transporters in plasma cell membranes and their proposed mode of action are described.
This chapter discusses the mammalian mitotic cell cycle, presents biotin as a model for studies of nutrient homeostasis in proliferating cells, and provides a review of recent studies that have directly addressed the interaction between cell proliferation and biotin metabolism.
This chapter discusses the metabolism of classically considered vitamins (vitamin A, vitamin D (calciferols), vitamin E, vitamin K, thiamin (B1), riboflavin (B2), niacin, vitamin B6, pantothenic acid, biotin, folic acid, vitamin B12 (cobalamins), vitamin C (L-ascorbic acid)) to physiologically active forms, i.e. coenzymes or hormones, and describes their subsequent compartmentalizations. Events covered are those that occur upon uptake through the plasma membrane of a eukaryotic cell, the subsequent partitioning into cytosol and organelles (mitochondria, endoplasmic reticulum, lysozomes, nucleus, etc.), and those metabolic alterations that are involved.
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