Separate and joint effects of arginine and glucose on ovine fetal insulin secretion

Gresores, A; Anderson, Susan M.; Hood, Darryl B.; Zerbe, Gary O.; Hay, William W.

doi:10.1152/ajpendo.1997.272.1.e68

Cited by 18 publications

(18 citation statements)

References 27 publications

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“…The neonatal insulin response to arginine was also consistently smaller than that to glucose throughout the 10-day period of the study. Although this may have been in part attributable to the decrease in plasma glucose, overall the current observations indicate that, in common with other species (Hermans et al 1987, Gresores et al 1997, arginine and glucose act through different mechanisms to stimulate the release of insulin from equine cells. The results also suggest that these two mechanisms are affected differentially by the nutritional adaptations at birth.…”

Section: Discussionmentioning

confidence: 47%

Development of insulin and proinsulin secretion in newborn pony foals

Holdstock

Allen²,

Bloomfield³

et al. 2004

Journal of Endocrinology

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At birth, the endocrine pancreas must assume a glucoregulatory role if the neonate is to survive the transition from parenteral to enteral nutrition. In species like the horse, neonatal hypoglycaemia is common, which suggests that the glucoregulatory mechanisms are not always fully competent at birth. Hence, this study examined pancreatic cell function in newborn foals during nutritional adaptation over the first 10 days post partum. Over a 48 h period at three time intervals after birth (days 1-2, 5-6 and 9-10 post partum), the cell responses to suckling and to intravenous administration of glucose, arginine and saline were measured in seven normal pony foals. Basal plasma concentrations of proinsulin, but not insulin or glucose, increased significantly between days 1 and 10. Suckling caused a gradual increase in plasma glucose, which was accompanied by a significant increase in plasma insulin concentrations 15 min after the onset of suckling on days 5 and 9, but not day 1. There was no significant change in plasma proinsulin concentrations in response to suckling at any age. At all ages studied, glucose and arginine administration stimulated an increase in the plasma concentrations of insulin and proinsulin; these cell responses did not change significantly with postnatal age. The insulin responses to glucose were significantly greater than those of arginine at each time period. Glucose clearance was significantly slower on day 1 than subsequently. Proinsulin and glucose, but not insulin, concentrations decreased significantly after saline administration at all three ages. At each time period, there was a significant positive relationship between the plasma insulin and proinsulin concentrations, the slope of which was significantly shallower on days 1-2 than subsequently. These results show that equine cells are responsive to glucose and arginine and release both insulin and proinsulin during the immediate postnatal period. They also suggest that newborn foals may be insulin resistant on the first day after birth.

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Section: Discussionmentioning

confidence: 47%

Development of insulin and proinsulin secretion in newborn pony foals

Holdstock

Allen²,

Bloomfield³

et al. 2004

Journal of Endocrinology

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“…The difference in the magnitude and time course of the fetal -cell response to arginine and glucose in this and previous studies of sheep and rats indicates that these two secretagogues also act through different mechanisms in utero (Gersch et al 1974, Fowden 1980a, Gresores et al 1997. In addition, the current observation that the fetal -cell response to glucose, but not arginine, increases with proximity to delivery suggests that prepartum maturation of the insulin secretory pathways occurs upstream of -cell depolarisation.…”

Section: Discussioncontrasting

confidence: 49%

“…The endocrine pancreas is functional before birth and secretes insulin in utero in response to glucose and amino acids in several species including the horse (Gersch et al 1974, Fowden 1980a,b, 1982a,b, Bassett et al 1982, Carver et al 1996, Gresores et al 1997, Aldoretta et al 1998. Fetal pancreatic cells also respond to neural stimulation and to circulating catecholamines during late gestation (Fowden 1980b, Sperling et al 1980, Lang et al 1993, Jackson et al 2000.…”

Section: Introductionmentioning

confidence: 99%

Maturation of pancreatic β-cell function in the fetal horse during late gestation

Fowden

Gardner²,

Ousey³

et al. 2005

Journal of Endocrinology

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At birth, the endocrine pancreas becomes more directly involved in the control of glycaemia than in utero. However, compared with other tissues, relatively little is known about the maturational changes that occur in the fetal endocrine pancreas in preparation for extrauterine life. This study examined the pancreatic -cell response to exogenous administration of glucose and arginine in fetal horses with respect to their gestational age and concentration of cortisol, the hormone responsible for prepartum maturation of other fetal tissues. Glucose administration had no effect on fetal insulin secretion between 175 and 230 days of gestation but evoked a rapid insulin response in fetuses closer to term (290-327 days). In late gestation, the -cell response was more rapid and greater in magnitude in fetuses with basal cortisol levels higher than 15 ng/ml than in those with lower cortisol values at the time of glucose administration. The fetal -cell response to arginine was unaffected by the rise in fetal plasma cortisol towards term. These findings show that there are maturational changes in pancreatic -cell function in fetal horses as cortisol levels rise close to term. Primarily, these prepartum maturational changes were in the mechanisms of glucose-stimulated insulin secretion, which would enable the cells to regulate glycaemia at the higher glucose levels observed postnatally.

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“…The mechanisms by which arginine promotes fetal growth, however, are multifaceted and have not been adequately investigated. Arginine is an insulin secretagogue in ovine and human fetuses (3)(4)(5)(6)(7) and in human newborns (8 -10); thus the role of arginine in fetal growth may include an insulin-mediated anabolic effect. In addition, arginine could stimulate growth as a precursor for polyamine synthesis (11) and nitric oxide production (12)(13)(14).…”

mentioning

confidence: 99%

Ovine Placental and Fetal Arginine Metabolism at Normal and Increased Maternal Plasma Arginine Concentrations

et al. 2002

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Arginine (A) may play a significant role in fetal growth, by stimulating insulin secretion and as a precursor for both polyamine synthesis and nitric oxide production. To determine whether increased maternal plasma A concentrations can enhance delivery of A to the fetus, uterine, umbilical, and net uteroplacental (UP) A uptake rates were measured in 12 pregnant ewes at 129.6 Ϯ 0.4 d gestation (mean Ϯ SEM) during normal and after 3 h of increased maternal plasma A concentrations. With a 2.7-fold increase in maternal plasma A concentrations (p Ͻ 0.001), there were significant increases in uterine A uptake (13.8 Ϯ 1.0 to 41.3 Ϯ 7.7 mol/min, p Ͻ 0.005), umbilical A uptake (3.3 Ϯ 0.5 to 5.2 Ϯ 0.8 mol·min Ϫ1 ·kg Ϫ1 fetus, p Ͻ 0.005), UP A uptake (17.8 Ϯ 6.2 to 89.2 Ϯ 20.3 mol·min Ϫ1 ·kg Ϫ1 placenta, p Ͻ 0.01), fetal arterial A concentration (98.7 Ϯ 6.3 to 137.1 Ϯ 9.9 M, p Ͻ 0.001), maternal A disposal rate (143.7 Ϯ 9.4 to 217.0 Ϯ 6.7 mol/min, p Ͻ 0.001), fetal A disposal rate (7.9 Ϯ 0.8 to 9.9 Ϯ 1.1 mol·min Ϫ1 ·kg Ϫ1 , p Ͻ 0.05), fetal A oxidation rate (1.31 Ϯ 0.24 to 1.84 Ϯ 0.36 mol·min Ϫ1 ·kg Ϫ1 , p Ͻ 0.05), and plasma insulin concentration in both fetus (16 Ϯ 2 to 20 Ϯ 2 U/mL, p Ͻ 0.001) and mother (24 Ϯ 3 to 32 Ϯ 4 U/mL, p Ͻ 0.001). Thus, increased maternal plasma A concentration increases maternal, UP, and fetal A net uptake, and increases insulin secretion in mother and fetus. The 4.2-fold larger increase in UP than net fetal A uptake could represent preferential UP A metabolism relative to fetal A metabolism, relatively limited placental-fetal A transport capacity compared with uterine A uptake capacity, or both; responsible mechanisms remain unknown. Arginine is a conditionally indispensable amino acid in the mammalian fetus and neonate (1, 2), and maintenance of fetal arginine supply and plasma concentrations are important for optimal fetal growth. The mechanisms by which arginine promotes fetal growth, however, are multifaceted and have not been adequately investigated. Arginine is an insulin secretagogue in ovine and human fetuses (3-7) and in human newborns (8 -10); thus the role of arginine in fetal growth may include an insulin-mediated anabolic effect. In addition, arginine could stimulate growth as a precursor for polyamine synthesis (11) and nitric oxide production (12-14).In contrast, arginine deficiency has been shown to induce growth restriction in experimental animals (15, 16). A potential therapy for fetal growth restriction, therefore, could include maternal plasma arginine supplementation in an attempt to increase fetal arginine supply. It is not known, however, whether increasing maternal plasma arginine concentration could increase net fetal arginine uptake, fetal plasma arginine concentration, or fetal insulin concentration. In addition, the characteristics of placental arginine uptake, metabolism, and transport to the fetus have not been determined. Therefore, this study was designed to determine how maternal arginine supplementation affects maternal, uteroplacental, and fetal arginine net ...

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Separate and joint effects of arginine and glucose on ovine fetal insulin secretion

Cited by 18 publications

References 27 publications

Development of insulin and proinsulin secretion in newborn pony foals

Development of insulin and proinsulin secretion in newborn pony foals

Maturation of pancreatic β-cell function in the fetal horse during late gestation

Ovine Placental and Fetal Arginine Metabolism at Normal and Increased Maternal Plasma Arginine Concentrations

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