Recent studies on the biological actions of vitamin D on intestinal transport and the electrophysiology of peripheral nerve and cardiac muscle.
Vitamin D, with parathyroid hormone and calcitonin, is an essential factor in the homeostatic regulation of systemic calcium in most vertebrate species. Targets for this aspect of vitamin D action, through its biologically active metabolites, are primarily the intestine, kidney and bone. Each of these tissues or organs are stimulated by 1,25(OH)2D3 to increase the transport calcium into the extracellular fluid compartment when plasma calcium levels are below normal and/or when there is a greater need for calcium to meet the requirements of physiological processes, such as growth, gestation and lactation. During such periods, the efficiency of the absorption of calcium from the intestine increases, the resorption of calcium salts from bone is stimulated, and the efficiency of the reabsorption of filtered calcium by the renal tubule is increased. In addition to the homeostatic function of vitamin D, there is an increasing amount of evidence that vitamin D has important effects on tissues and organs other than those concerned with calcium homeostasis. With regard to the intestinal epithelial system, the genomic effect of 1,25(OH)2D3 was shown several years ago when the de novo synthesis of a specific vitamin D-induced calcium-binding protein (CaBP, calbindin-D) was demonstrated. In our view, this appears to be an essential factor in the well-documented enhancement of calcium absorption by vitamin D. The function of calbindin-D, a high affinity calcium-binding protein, in the absorptive process is not precisely known but currently considered to act as an intracellular facilitator of the diffusion of calcium from the microvillar pole of the enterocyte to the basal-lateral membrane. There is evidence that vitamin D influences another step in the absorptive process. This step appears to be associated with the entrance of luminal calcium into the enterocyte, the first step in the transepithelial transport process. This response appears to occur relatively early (1 h or less) after 1,25(OH)2D3 is given to vitamin D-deficient animals, whereas the de novo synthesis of transport proteins has a much longer lag time (about 4 h). The in vitro absorption studies of Nemere et al (1984) and the in vivo experiments of our group (Wasserman et al, 1982) accentuate this point. However, the more rapid reaction, i.e., the possible modification of the permeability properties of the brush border membrane, does not result in a substantive increase in overall calcium absorption unless the enterocyte had been "primed" by previous exposure to vitamin D. The "priming" reaction might represent the synthesis of CaBP or some other intracellular component.(ABSTRACT TRUNCATED AT 400 WORDS)
Department of Physiology, New York State College of Veterinary Medicine, Cornell University, Ithaca 14853.
R H
RH
Wasserman
M E
ME
Brindak
M M
MM
Buddle
Q
Q
Cai
F C
FC
Davis
C S
CS
Fullmer
R F
RF
Gilmour
C
C
Hu
H M
HM
Mykkanen
D N
DN
Tapper
D000818:Animals; D001427:Bacterial Toxins / Q000494:pharmacology; D002136:Calcium, Dietary / Q000378:metabolism; D002645:Chickens; D004768:Enterotoxins / Q000494:pharmacology; D029968:Escherichia coli Proteins; D007408:Intestinal Absorption / Q000187:drug effects*; D008274:Magnesium / Q000378:metabolism; D008871:Microvilli / Q000378:metabolism; D009200:Myocardial Contraction / Q000187:drug effects; D009431:Neural Conduction / Q000187:drug effects*; D010525:Peripheral Nerves / Q000187:drug effects; D013438:Sulfhydryl Compounds / Q000378:metabolism; D014807:Vitamin D / Q000494:pharmacology*; D014808:Vitamin D Deficiency / Q000503:physiopathology
D001427:Bacterial Toxins; D002136:Calcium, Dietary; D004768:Enterotoxins; D029968:Escherichia coli Proteins; D013438:Sulfhydryl Compounds; C034151:heat stable toxin (E coli); D014807:Vitamin D; D008274:Magnesium