The Impact of Euglycemia and Hyperglycemia on Stimulated Pituitary Hormone Release in Insulin- Dependent Diabetics*
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To study the influence of different blood glucose (BG) concentrations on the release of pituitary hormones, the effect of the simultaneous iv administration of LRH (200 micrograms), TRH (400 micrograms), and arginine (30 g/30 min) upon the serum concentrations of LH, FSH, TSH, PRL, and GH was determined in six male insulin-dependent diabetics. BG concentration was clamped by feedback control and an automated glucose-controlled insulin infusion system at euglycemic (BG 4-5 mmol/liter) or hyperglycemic (BG, 14-18 mmol/liter) levels. Increments in serum concentrations of LH, FSH, TSH, and PRL were similar in the euglycemic and hyperglycemic steady states, whereas the GH response to arginine was suppressed during the hyperglycemic clamp (P less than 0.01). Omission of exogenous insulin during hyperglycemia did not modify the observed hormonal responses. Thus, the release of LH, FSH, TSH, and PRL in response to adequate acute stimuli at the pituitary level is not modulated by hyperglycemia in insulin-dependent diabetes, while arginine-induced GH release is suppressed. Since the effect of arginine on GH is most likely mediated by an action on the hypothalamus, the data suggest that elevated glucose concentrations may exert their modulatory influence on GH secretion at the hypothalamic rather than at the pituitary level.The effect of carbohydrate on arginine utilization by excised bean (Phaseolus vulgaris L. var. Tendergreen) leaves in the dark was studied by adding arginine to leaves differing in carbohydrate levels, and measuring the arginine content of the leaves at intervals. In nonstarved leaves, the arginine content decreased steadily after vacuum infiltration of 10 mm arginine and was essentially completely utilized by 36 hours after infiltration. In starved leaves, the arginine content did not decrease except for a brief period of about 4 hours after infiltration. The distribution of 14C after adding 14C-arginine to starved and nonstarved leaves indicated that the presence of carbohydrates in the leaves stimulates the utilization of arginine for protein synthesis and conversion to other amino acids, organic acids, and CO2 (catabolism). Adding sucrose along with arginine to starved leaves stimulated this utilization of arginine for both protein synthesis and catabolism. This effect of sugar on catabolism is different than results of similar studies done previously with proline. Increasing the concentration of added arginine greatly increased arginine catabolism but had a relatively small effect on utilization of arginine for protein synthesis. This result is the same as similar results from adding different concentrations of proline to excised leaves.
Catabolism
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Arginine is conditionally indispensable in the neonate, and its synthesis in the intestine is not sufficient to meet requirements. It is not known how neonatal endogenous arginine synthesis is regulated and the degree to which proline and glutamate are used as precursors. Primed, constant intraportal and intragastric infusions of L-[U-14C]proline and L-[3,4-3H]glutamate, and intragastric L-[guanido-14C]arginine were used to measure whole body and first-pass intestinal arginine synthesis in 10 neonatal piglets fed generous (1.80 g.kg(-1).day(-1)) or deficient (0.20 g.kg(-1).day(-1)) quantities of arginine for 5 days. Glutamate tracer was not detected in arginine, indicating a biologically insignificant conversion of <1% of arginine flux. Endogenous arginine synthesis from proline had obligatory (0.36 g.kg(-1).day(-1)) and maximal (0.68 g.kg(-1).day(-1)) levels (P < 0.05, pooled SE 0.05). Although first-pass gut metabolism is responsible for 42-63% of whole body arginine synthesis, the gut is incapable of upregulating proline to arginine conversion during arginine deficiency, compared with a more than threefold increase without first-pass gut metabolism. These data suggest that upregulation of proline-to-arginine conversion occurs via increased arterial extraction of proline by the gut or in nonintestinal tissues. This study demonstrates that dietary arginine is an important regulator of endogenous arginine synthesis in the neonatal piglet and that proline, but not glutamate, is an important precursor for arginine synthesis in the neonate.
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The role of the hypothalamus in the control of body temperature can be studied by a number of different methods, e.g.: 1. Destruction of hypothalamic areas; 2. Electrical stimulation of the hypothalamus; 3. Heating or cooling of the hypothalamus; 4. Studies of the biochemistry of the hypothalamus; 5. Injection of pharmacological agents into the third ventricle or into the hypothalamus; 6. Recording of the electrical activity of hypothalamic neurons during heating and cooling of the brain. We will review the evidence that has been gathered using these techniques, and we will attempt to interpret the results in comparison with the more thoroughly studied mammalian hypothalamic thermoregulatory control system. Destruction of Hypothalamic Areas. Care should be taken to ascertain that the effects observed are the result of destruction per se and are not the result of iron deposits from stainless steel electrodes. It has been shown, for instance, that lesions in . . .
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The role of guanidinoacetic acid (GAA) and its relationship with arginine was reviewed in order to define a replacement ratio between GAA and arginine for broiler diet formulation, the ratio being of how much arginine could be spared, or replaced by GAA. Guanidionoacetic acid, the precursor of creatine, can be synthesized de novo from the amino acids arginine and glycine, whereby 1 mol of arginine creates 1 mol of GAA; that is a weight:weight (w:w) ratio of 1.49:1 (arginine:GAA). Guanidinoacetic acid exerts a growth effect through its primary physiological fate to form creatine, and additionally spares dietary arginine from GAA synthesis; so that it contributes to protein accretion and other functions. Creatine is critical in energy metabolism as a carrier and reservoir of phosphate for adenosine triphosphate (ATP) formation. Arginine deficiency causes reduced growth and can lead to disrupted levels of blood and muscle energy metabolites (phosphocreatine and creatine). Supplementing GAA into the diet restores these metabolites. At severe arginine deficiency, GAA addition cannot fully compensate the arginine deficit, as measured by growth performance. As arginine becomes nearer to sufficiency, the effect of GAA becomes more pronounced. When using growth rate or FCR as an indicator in broilers, a ratio in the range of 0.77 to 1.3:1 (w:w arginine:GAA) was seen, with one study noting a ratio of 2:1 when using FCR as an indicator. Higher ratios of up to 2.7:1 are achieved when using muscle creatine and phosphocreatine measurements. A recommendation of 1:1 (w:w) is proposed, which takes a conservative approach. Large scale studies with practical diets would be helpful to confirm that a ratio of 1:1 (w:w) or higher may be used in the field for broilers.
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We have shown that first-pass intestinal metabolism is necessary for approximately 50% of whole body arginine synthesis from its major precursor proline in neonatal piglets. Furthermore, the intestine is not the site of increased arginine synthesis observed during dietary arginine deficiency. Primed constant intravenous (iv) and intraportal (ip) infusions of L-[U-14C]proline, and iv infusion of either L-[guanido-14C]arginine or L-[4,5-3H]arginine were used to measure first-pass hepatic arginine synthesis in piglets enterally fed either deficient (0.20 g.kg(-1).day(-1)) or generous (1.80 g.kg(-1).day(-1)) quantities of arginine for 5 days. Conversion of arginine to other urea cycle intermediates and arginine recycling were also calculated for both dietary treatments. Arginine synthesis (g.kg(-1).day(-1)) from proline was greater in piglets (P < 0.05) fed the deficient arginine diet in both the presence (generous: 0.07; deficient: 0.17; pooled SE = 0.01) and absence (generous: 0.06; deficient: 0.20; pooled SE = 0.01) of first-pass hepatic metabolism. There was no net arginine synthesis from proline during first-pass hepatic metabolism regardless of arginine intake. Arginine conversion to urea, citrulline, and ornithine was significantly greater (P < 0.05) in piglets fed the generous arginine diet. Calculated arginine fluxes were significantly lower (P = 0.01) for [4,5-3H]arginine than for [guanido-14C]arginine, and the discrepancy between the values was greater in piglets fed the deficient arginine diet (35% vs. 20%). Collectively, these findings show that first-pass hepatic metabolism is not a site of net arginine synthesis and that piglets conserve dietary arginine in times of deficiency by decreasing hydrolysis and increasing recycling.
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AIM To research the functions of rat hypothalamus under long term simulated weightlessness condition. METHODS By using anti Fos and anti GFAP immunohistochemical ABC methods, we observed changes of hypothalamus neurons and astrocytes in 4 wk simulated rats. RESULTS Expressions of Fos and GFAP positive cells were only found in paravetricular nuclei of the hypothalamus, especially in mango cellular part, supraoptic nuclei and suprachiasmatic nuclei, with negative reaction in other areas. The reactive astrocytes were featured with hypertrophy of the cell body and cytoplasmic processes. CONCLUSION These nuclei in hypothalamus may participate in the reaction to long term weightlessness, and probably be associated with increased secretion of vasopressure.
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l -Arginine hydroxamate inhibited the growth of various bacteria, and the inhibition was readily reversed by arginine. l -Arginine hydroxamate (10 −3 m ) completely inhibited the growth of Bacillus subtilis . This inhibitory effect was prevented by 2.5 × 10 −4 m l -arginine, which was the most effective of all the natural amino acids in reversing the inhibition. l -Arginine hydroxamate-resistant mutants of Bacillus subtilis were isolated and found to excrete l -arginine in relatively high yields. One of the mutants, strain AHr-5, produced 4.5 mg of l -arginine per ml in shaken culture in 3 days.
Strain (injury)
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Arginine serves multiple roles in the pathophysiological response to burn injury. Our previous studies in burn patients demonstrated a limited net rate of arginine de novo synthesis despite a significantly increased arginine turnover (flux), suggesting that this amino acid is a conditionally indispensable amino acid after major burns. This study used [ 15 N 2 -guanidino-5,5- 2 H 2 ]arginine and [5- 13 C]ornithine as tracers to assess the rate of arginine disposal via its conversion to and subsequent oxidation of ornithine; [5,5- 2 H 2 ]proline and [5,5,5- 2 H 3 ]leucine were also used to assess proline and protein kinetics. Nine severely burned patients were studied during a protein-free fast (“basal” or fast) and total parenteral nutrition (TPN) feedings. Compared with values from healthy volunteers, burn injury significantly increased 1) fluxes of arginine, ornithine, leucine, and proline; 2) arginine-to-ornithine conversion; 3) ornithine oxidation; and 4) arginine oxidation. TPN increased arginine-to-ornithine conversion and proportionally increased irreversible arginine oxidation. The elevated arginine oxidation, with limited net de novo synthesis from its immediate precursors, further implies that arginine is a conditionally indispensable amino acid in severely burned patients receiving TPN.
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