Physiologic regulation in electromagnetic fields

Electromagnetic fields have been demonstrated to elicit thermoregulatory responses, neuroen-docrine, neurochemical modulations, and behavioral reactions. These physiologic regulatory processes are exquisitely tuned, interrelated functions that constitute sensitive indicators of organismic responses to radiofrequency energy absorption (the radio frequency portion of the electromagnetic spectrum includes as one part microwaves). Assessment of the integration and correlation of these functions relative to the thermal inputs and homeokinetic reactions of the individual subjected to radiofrequency energy should permit differentiation between potential hazards that might compromise the individual's ability to maintain normal physiologic function and effects that are compensated by physiologic redundancy.     

Physiologic aspects of pyridine nucleotide regulation in mammals

Summary Tissue levels of NAD⁺ appear to be regulated primarily by the concentration of extracellular nicotinamide, which in turn is controlled by the liver in a hormone-sensitive manner. Hepatic regulation involves the conversion of excess serum nicotinamide to Storage NAD⁺ and inactive excretory products, and the replenishment of serum nicotinamide by the hydrolysis of Storage NAD⁺. Tryptophan and nicotinic acid contribute to Storage NAD⁺, and thus are additional sources of nicotinamide. In response to administered nicotinamide, there is a preferential utilization of ATP and PRPP (5-phosphorylribose-1-pyrophosphate) for the biosynthesis of NAD⁺. This biosynthetic priority, whose purpose appears to be the conservation of intracellular nicotinamide, may explain why nicotinamide inhibits RNA and DNA synthesis in regenerating tissues and why elevated nicotinamide levels are toxic to growing animals and to mammalian cells in culture.     

Cellular regulation of human lymphocyte mitogenic factor release in vitro]

Production of the mitogenic facotr by human lymphocytes stimulated with phytohemagglutinin (PHA) was investigated. Anti-PHA antibodies were used for studying the culture medium mitogenic activity. The mitogenic factor production markedly increased after lymphocyte irradiation. When macrophages were eliminated, using iron powder, mitogenic factor generation was also increased. It was demonstrated that lymphocyte irradiation and macrophage elimination stimulated the mitogenic factor production throgh different mechanisms.     

Mitochondrial regulation of insulin action

Insulin resistance is the prodrome of many metabolic diseases and identifying ways to correct this pathological condition is a major goal for medical research. The foremost barrier to the development of new treatments is that the precise etiology of insulin resistance is uncertain. Recent studies suggest that changes in mitochondrial structure or function drive this condition, however much of this evidence is circumstantial. This Signaling Networks in Focus article provides a brief overview of known and speculative regulatory intersections whereby mitochondrial dysfunction at the levels of lipid oxidation, oxidative stress, calcium, adenine nucleotides, and protons may regulate insulin sensitivity. If mitochondrial dysfunction underlies the origins of metabolic disease then determining the precise molecular pathway will be essential for the development of new treatment and prevention strategies.     

Comparison of models of insulin release

A model for insulin secretion with a storage and a labile compartment, as well as a provisionary factor, is combined with a signal model in which the signal can be the difference between an excitation and an inhibition, or the difference in concentrations inside and outside some cell components. The model, using a single set of values for the parameters, accounts in a semiquantitative manner for all of the regularly appearing features of the insulin secretion from thein vitro perfused pancreas to a wide range of patterns of glucose and tolbutamide stimulation. Among the features which can be accounted for are: early and late secretion of insulin as a function of glucose in terms of a single parameter; the apparent depletion and recovery during a pulsed pattern of stimulation by tolbutamide; the hypersecretion following a short period of rest during a prolonged stimulation by glucose; the negative spike which occurs when the concentration of glucose, which has been maintained for a period of time, is suddenly reduced to a lower level; and the appropriate responses to slow and fast ramp functions of glucose concentration.     

Physiologic regulation of mixtalol in rape senescence and its yield effects

Physiologic and yield effects of mixtalol at various concentrations sprayed on rape at the anthesis stage were examined. Foliar sprays of 4 and 2 ppm mixtalol significantly increased the chlorophyll content of rape leaves and pods, reduced the accumulation of malondialdehyde and ethylene production, and delayed the degradation of superoxide dismutase and catalase activities of the rape plant. Mixtalol also increased root oxidizability. Meanwhile, the number of branches and pods per plant was increased, and a 10.7% and 8.2% increase of seed yield over the controls was observed with treatments of 4 and 2 ppm mixtalol, respectively. No significant effects from mixtalol were observed on the maturation of plants or on the seed oil content or the erucic acid and glucosinolate content. Total rape oil production increased with 4 and 2 ppm mixtalol significantly by 12.4% and 10.5%, respectively, over the controls.Abbreviations MTL mixtalol - MDA malondialdehyde - TBA thiobarbituric acid - SOD Superoxide dismutase - CAT catalase - TTC tetrazolium     

Stimulation of insulin release by L-glutamine

Summary Under normal environmental conditions, L-glutamine is well oxidized but fails to stimulate insulin release in rat pancreatic islets. However, a marked stimulation of insulin release by L-glutamine, without alteration in its oxidation rate, occurs when the intracellular pH of the islet cells is decreased and/or when theophylline is added to the incubation medium.     

Measuring the balance between insulin synthesis and insulin release

The absolute rates of hormone synthesis and release were determined in purified pancreatic B cells. Newly synthesized proteins were labeled with L-[3,5-3H]tyrosine or L-[2,5-3H]histidine. When medium glucose was less than or equal to 10 mM, the production of insulin exceeded or equaled its release. Raising the glucose levels above 10 mM did not further increase the rate of insulin synthesis (67 +/- 10 fmol/10(3) cells/2 hour) but elevated that of insulin release up to 3-fold the production rates (181 +/- 10 fmol/10(3) cells/2 hour). In the presence of glucagon or of the phorbol ester 12-O-tetradecanoylphorbol 13-acetate the cells also released 3-fold more hormone that they synthesized; release was however reduced to 25% of the rate of production in the presence of epinephrine. It is concluded that glucose as well as hormonal regulators of islet B cells can influence, bi-directionally, the balance between the rates of insulin synthesis and release.     

Stimulation of insulin release by calcium

In the absence of secretagogue, Ca²⁺ (2 to 10 mM) provokes a short-lived release of insulin in the perfused rat pancreas first exposed to EGTA. The secretory response is abolished by verapamil and enhanced by theophylline. These findings afford the first demonstration that Ca²⁺ itself can trigger insulin release.     

Potentiation of glucose-induced insulin release in islets by desHis1[Glu9]glucagon amide

Glucagon and secretin and some of their hybrid analogs potentiate glucose-induced release of insulin from isolated mouse pancreatic islets. It was recently shown that the synthetic glucagon analog, desHis1[Glu9]glucagon amide, does not stimulate the formation of cyclic adenosine monophosphate in the rat hepatocyte membrane, but binds well to the glucagon receptor and is a good competitive antagonist of glucagon. In the present study the effect of this analog on isolated islets was examined. desHis1-[Glu9]glucagon amide at 3 x 10(-7) M, in the presence of 0.01 M D-glucose, increased the release of insulin by 30% and maintained that level for the full 30-min test period. The rate of insulin release returned to the glucose-induced base line after removal of the peptide. The same insulin level was produced by 3 x 10(-9) M glucagon, and at 3 x 10(-7) M glucagon insulin release was enhanced 290% above the glucose base line.