Effects of body temperature maintenance on glucose, insulin, and corticosterone responses to acute hypoxia in the neonatal rat

2012 ◽  
Vol 302 (5) ◽  
pp. R627-R633 ◽  
Author(s):  
Mitchell A. Guenther ◽  
Eric D. Bruder ◽  
Hershel Raff
Keyword(s):  
Glucose Homeostasis ◽  
Plasma Glucose ◽  
Acute Hypoxia ◽  
Insulin Response ◽  
Plasma Corticosterone ◽  
Neonatal Rat ◽  
Control Group ◽  
Initial Increase ◽  
Time Control ◽  
Subsequent Decrease

One of the biggest challenges of premature birth is acute hypoxia. Hypothermia during acute hypoxic periods may be beneficial. We hypothesized that prevention of hypothermia during neonatal hypoxia disrupts glucose homeostasis and places additional metabolic challenges on the neonate. Pups at PD2 and PD8 were exposed to 8% O2 for 3 h, during which they were allowed to either spontaneously cool or were kept isothermic. There was also a time control group that was subjected to normoxia and kept isothermic. Plasma glucose, insulin, C-peptide, corticosterone, and catecholamines were measured from samples collected at baseline, 1 h, 2 h, and 3 h. In postnatal day 2 (PD2) rats, hypoxia alone resulted in no change in plasma glucose by 1 h, an increase by 2 h, and a subsequent decrease below baseline values by 3 h. Hypoxia with isothermia in PD2 rats elicited a large increase in plasma insulin at 1 h. In PD8 rats, hypoxia with isothermia resulted in an initial increase in plasma glucose, but by 3 h, glucose had decreased significantly to below baseline levels. Hypoxia with and without isothermia elicited an increase in plasma corticosterone at both ages and an increase in plasma epinephrine in PD8 rats. We conclude that the insulin response to hypoxia in PD8 rats is associated with an increase in glucose similar to an adult; however, insulin responses to hypoxia in PD2 rats were driven by something other than glucose. Prevention of hypothermia during hypoxia further disrupts glucose homeostasis and increases metabolic challenges.

Adrenocorticotropic hormone and corticosterone responses to acute hypoxia in the neonatal rat: effects of body temperature maintenance

2011 ◽  
Vol 300 (3) ◽  
pp. R708-R715 ◽  
Author(s):  
Eric D. Bruder ◽  
Kimberli J. Kamer ◽  
Mitchell A. Guenther ◽  
Hershel Raff
Keyword(s):  
Stress Response ◽  
Body Temperature ◽  
Acute Hypoxia ◽  
Plasma Corticosterone ◽  
Neonatal Rat ◽  
Plasma Acth ◽  
Neonatal Hypoxia ◽  
Rat Pups ◽  
Expression Of Genes ◽  
Corticosterone Response

The corticosterone response to acute hypoxia in neonatal rats develops in the 1st wk of life, with a shift from ACTH independence to ACTH dependence. Acute hypoxia also leads to hypothermia, which may be protective. There is little information about the endocrine effects of body temperature maintenance during periods of neonatal hypoxia. We hypothesized that prevention of hypothermia during neonatal hypoxia would augment the adrenocortical stress response. Rat pups separated from their dams were studied at postnatal days 2 and 8 ( PD2 and PD8). In one group of pups, body temperature was allowed to spontaneously decrease during a 30-min prehypoxia period. Pups were then exposed to 8% O2 for 3 h and allowed to become spontaneously hypothermic or externally warmed (via servo-controlled heat) to maintain isothermia. In another group, external warming was used to maintain isothermia during the prehypoxia period, and then hypoxia with or without isothermia was applied. Plasma ACTH and corticosterone and mRNA expression of genes for upstream proteins involved in the steroidogenic pathway were measured. Maintenance of isothermia during the prehypoxia period increased baseline plasma ACTH at both ages. Hypothermic hypoxia caused an increase in plasma corticosterone; this response was augmented by isothermia at PD2, when the response was ACTH-independent, and at PD8, when the response was ACTH-dependent. In PD8 rats, isothermia also augmented the plasma ACTH response to hypoxia. We conclude that maintenance of isothermia augments the adrenocortical response to acute hypoxia in the neonate. Prevention of hypothermia may increase the stress response during neonatal hypoxia, becoming more pronounced with increased age.

scholarly journals Acute hypoxia and endogenous renal endothelin.

1994 ◽  
Vol 4 (11) ◽  
pp. 1920-1924
Author(s):  
A Nir ◽  
A L Clavell ◽  
D Heublein ◽  
L L Aarhus ◽  
J C Burnett
Keyword(s):  
Acute Hypoxia ◽  
Fractional Excretion ◽  
Urinary Sodium Excretion ◽  
Renal Tissue ◽  
Control Group ◽  
Moderate Hypoxia ◽  
Time Control ◽  
Fractional Excretion Of Sodium ◽  
Air Ventilation ◽  
Hypoxic Group

Endothelin (ET) is a potent vasoconstrictor peptide of endothelial cell origin. Recent studies have suggested a nonvascular paracrine and/or autocrine role for endothelin in the kidney. This study was designed to elucidate the renal ET response to acute moderate hypoxia, as reflected by urinary ET excretory rate and renal tissue ET immunoreactivity, and to correlate these responses to the hemodynamic and excretory changes during hypoxia. Experiments were conducted in two groups of anesthetized dogs: hypoxic group (10% O2 ventilation: PO2, 44 mm Hg; N = 7) and time control group (room air ventilation: PO2, 111 mm Hg; N = 6). After 60 min of hypoxia or room air ventilation, kidneys were harvested and stained immunohistochemically for ET. Acute moderate hypoxia was associated with significant increases in urinary ET excretion, urine flow, urinary sodium excretion, and fractional excretion of sodium (P < 0.05). There was no significant change in GFR, RBF, renal vascular resistance, or mean arterial pressure. Renal immunohistochemistry for ET revealed increased staining in the proximal and distal tubules in the hypoxic group as compared with controls. This study demonstrates that acute moderate hypoxia results in increased urinary ET excretion and renal tubular ET immunoreactivity, in association with diuresis and natriuresis, and suggests a nonvascular role of endogenously produced renal ET in the regulation of sodium homeostasis during hypoxia.

Glucose tolerance in early pregnancy

1986 ◽  
Vol 112 (2) ◽  
pp. 263-266 ◽  
Author(s):  
Inge Buch ◽  
Peter J. Hornnes ◽  
Claus Kühl
Keyword(s):  
Glucose Tolerance ◽  
Glucose Homeostasis ◽  
Early Pregnancy ◽  
Plasma Glucose ◽  
Fasting Plasma Glucose ◽  
Post Partum ◽  
Insulin Response ◽  
Oral Glucose ◽  
Plasma Glucagon ◽  
Fasting Plasma

Abstract. The effect of pregnancy on oral glucose tolerance (50 g of glucose) and plasma insulin and glucagon responses to oral glucose was studied in weeks 10 and 32 of pregnancy and again 1 year post partum in 12 normal women. Already in week 10, fasting plasma glucose was decreased and the glucose-induced insulin secretion increased as compared with post partum. However, glucose tolerance was not affected at this time. In week 32, glucose tolerance had deteriorated, although the levels of both fasting and glucose-induced insulin were higher than those found in early pregnancy and post partum. At all investigations fasting plasma glucagon and the suppression of plasma glucagon after oral glucose were similar, indicating that glucagon is not implicated in the changes in glucose homeostasis seen in pregnancy. It is concluded that glucose tolerance is unaltered by pregnancy in week 10. Pregnancy has, however, at this very early stage already affected glucose homeostasis as seen by the decrease in fasting plasma glucose and the increase in the insulin response to glucose.

scholarly journals Influence of low- and high-protein diets on glucose homeostasis in the rat

1988 ◽  
Vol 60 (3) ◽  
pp. 509-516 ◽  
Author(s):  
W. Okitolonda ◽  
S. M. Brichard ◽  
A. M. Pottier ◽  
J. C. Henquin
Keyword(s):  
Glucose Homeostasis ◽  
Plasma Glucose ◽  
Control Diet ◽  
Protein Energy Malnutrition ◽  
Insulin Response ◽  
High Protein Diet ◽  
High Protein ◽  
Oral Glucose ◽  
Insulin Levels ◽  
Energy Deprivation

1. The influence of the protein content of the diet on glucose homeostasis was studied in the rat. Rats of 28 d of age received ad lib. a control diet containing (g/kg) 150 protein (P15), or a diet containing 50 protein (P5) or 450 protein (P45). Since P5 rats spontaneously reduced their food intake, a fourth group of rats (P25) received the same amount of energy as P5 rats and the same amount of protein as P15 rats.2. After 12–13 weeks on these diets, plasma glucose and insulin levels were similar in fed P45, P25 and control P15 rats, but were lower in P5 rats. In fasted animals, plasma glucose and insulin levels were also decreased in P5 rats, whereas plasma glucose levels were increased in both P45 and P25 animals.3. During an oral glucose tolerance test, the glucose rise was only slightly larger in P5 than in P15 rats in spite of a considerably smaller increase in insulin levels. P45 rats displayed a normal tolerance to glucose with a normal insulin response, whereas tolerance to glucose was slightly poorer in P25 rats in spite of a normal insulin response.4. Pancreatic insulin stores were lower in P5 than in control P15 rats, not only because of the smaller size of their pancreas, but also because of a decrease in the insulin concentration in the gland. A much smaller decrease was also observed in P25 rats, whereas insulin reserves were not altered in P45 rats.5. It is concluded that the changes in glucose homeostasis observed in protein-energy malnutrition (P5 rats) are due to protein deprivation rather than to energy deprivation. A high-protein diet has little influence on glucose homeostasis in the rat.

scholarly journals Chronic Sleep Disturbance Impairs Glucose Homeostasis in Rats

2010 ◽  
Vol 2010 ◽  
pp. 1-6 ◽  
Author(s):  
R. Paulien Barf ◽  
Peter Meerlo ◽  
Anton J. W. Scheurink
Keyword(s):  
Body Weight ◽  
Sleep Disturbance ◽  
Glucose Homeostasis ◽  
Weight Control ◽  
Insulin Response ◽  
Glucose Regulation ◽  
Sleep Restriction ◽  
Control Group ◽  
Intravenous Glucose ◽  
Increased Risk

Epidemiological studies have shown an association between short or disrupted sleep and an increased risk for metabolic disorders. To assess a possible causal relationship, we examined the effects of experimental sleep disturbance on glucose regulation in Wistar rats under controlled laboratory conditions. Three groups of animals were used: a sleep restriction group (RS), a group subjected to moderate sleep disturbance without restriction of sleep time (DS), and a home cage control group. To establish changes in glucose regulation, animals were subjected to intravenous glucose tolerance tests (IVGTTs) before and after 1 or 8 days of sleep restriction or disturbance. Data show that both RS and DS reduce body weight without affecting food intake and also lead to hyperglycemia and decreased insulin levels during an IVGTT. Acute sleep disturbance also caused hyperglycemia during an IVGTT, yet, without affecting the insulin response. In conclusion, both moderate and severe disturbances of sleep markedly affect glucose homeostasis and body weight control.

Effect of exercise training and chronic glyburide treatment on glucose homeostasis in diabetic rats

1992 ◽  
Vol 72 (1) ◽  
pp. 143-148 ◽  
Author(s):  
L. J. Goodyear ◽  
M. F. Hirshman ◽  
E. D. Horton ◽  
E. S. Horton
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Glucose Tolerance ◽  
Glucose Homeostasis ◽  
Plasma Glucose ◽  
Insulin Response ◽  
Diabetic Rats ◽  
Oral Glucose ◽  
Oral Glucose Tolerance ◽  
Glucose Clearance

Exercise training and sulfonylurea treatment, either individually or in combination, were evaluated for their effects on plasma glucose concentrations, oral glucose tolerance, and glucose clearance in the perfused hindquarter of diabetic rats. Female rats that were injected with streptozocin (45 mg/kg iv) and had plasma glucose concentrations between 11 and 25 mM were considered diabetic and divided into sedentary, glyburide-treated, exercise-trained, and glyburide-treated plus exercise-trained groups. The sedentary streptozocin-treated rats were severely diabetic, as indicated by elevated glucose concentrations, impaired insulin response during oral glucose tolerance tests, and lower rates of glucose clearance in hindlimb skeletal muscle. Neither 8 wk of exercise training nor 4 wk of glyburide treatment alone improved these parameters. In contrast, the diabetic rats that were both trained and treated with glyburide showed some improvement in glucose homeostasis, as evidenced by lower plasma glucose concentrations, an enhanced insulin response to an oral glucose load, and a decrease in the severity of skeletal muscle insulin resistance compared with the diabetic controls. These data suggest that glyburide treatment or exercise training alone does not alter glucose homeostasis in severely insulin-deficient diabetic rats; however, the combination of exercise training and glyburide treatment may interact to improve glucose homeostasis in these animals.

Insulin action and dynamics modelled in patients taking the anabolic steroid methandienone (Dianabol)

1986 ◽  
Vol 71 (6) ◽  
pp. 665-673 ◽  
Author(s):  
I. F. Godsland ◽  
N. M. Shennan ◽  
V. Wynn
Keyword(s):  
Insulin Resistance ◽  
Insulin Secretion ◽  
Glucose Tolerance ◽  
Anabolic Steroid ◽  
Plasma Glucose ◽  
Insulin Response ◽  
Glucose Disposal ◽  
Initial Increase ◽  
Second Phase ◽  
Minimal Models

1. Plasma glucose and insulin concentrations were measured during oral (OGTT) and intravenous (IVGTT) glucose tolerance tests in nine patients off- and on-treatment with the anabolic steroid, methandienone (Dianabol). 2. On-treatment, the tolerance tests showed a markedly increased insulin response accompanied by impairment of glucose tolerance, characteristics normally attributed to insulin resistance. However, fasting plasma glucose (FPG) and insulin (FPI) concentrations were significantly reduced, whereas the pattern normally associated with insulin resistance is for both to be raised. 3. IVGTT glucose and insulin profiles were analysed using an algorithm derived from the minimal models of glucose and insulin dynamics originally proposed by R. Bergman and co-workers. Measures for the following parameters were thus obtained: Si, the sensitivity of glucose disposal to insulin; Sg, net insulin independent glucose disposal; ϕ1, the integral concentration of insulin delivered during the first phase of insulin secretion relative to the initial increase in glucose concentration above a model-derived threshold; ϕ2 the sensitivity of the rate of rise of insulin concentration in the second phase of insulin secretion to the concentration of glucose above a model-derived threshold; κ, the fractional clearance rate of insulin; and tl/2, the insulin half-life. 4. Si was significantly reduced on treatment by a factor of 4. Sg, ϕ1, ϕ2 and t1/2 were all significantly increased, and κ was significantly reduced. The increases in Sg and ϕ1 both showed significant correlations with the increase in weight on-treatment. 5. The reduction in FPG and FPI can be explained by the combined effects of the increase in Sg and Dianabol-induced resistance to glucagon. 6. Application of the Bergman models proved to be of value in identifying and quantifying Dianabol-induced insulin resistance. Model-derived parameters of insulin clearance and net insulin independent glucose uptake were also of use in interpreting the changes in glucose and insulin concentrations observed. However, model-derived parameters of pancreatic insulin secretion were likely to have been confounded by reduced hepatic insulin uptake associated with a state of relative insulin resistance.

scholarly journals Development of the ACTH and corticosterone response to acute hypoxia in the neonatal rat

2008 ◽  
Vol 295 (4) ◽  
pp. R1195-R1203 ◽  
Author(s):  
Eric D. Bruder ◽  
Jennifer K. Taylor ◽  
Kimberli J. Kamer ◽  
Hershel Raff
Keyword(s):  
Body Temperature ◽  
Acute Hypoxia ◽  
Age Groups ◽  
Thermal Response ◽  
Plasma Corticosterone ◽  
Neonatal Rat ◽  
Severe Hypoxia ◽  
Developmentally Regulated ◽  
Specific Proteins ◽  
Corticosterone Response

Acute episodes of severe hypoxia are among the most common stressors in neonates. An understanding of the development of the physiological response to acute hypoxia will help improve clinical interventions. The present study measured ACTH and corticosterone responses to acute, severe hypoxia (8% inspired O2 for 4 h) in neonatal rats at postnatal days (PD) 2, 5, and 8. Expression of specific hypothalamic, anterior pituitary, and adrenocortical mRNAs was assessed by real-time PCR, and expression of specific proteins in isolated adrenal mitochondria from adrenal zona fascisulata/reticularis was assessed by immunoblot analyses. Oxygen saturation, heart rate, and body temperature were also measured. Exposure to 8% O2 for as little as 1 h elicited an increase in plasma corticosterone in all age groups studied, with PD2 pups showing the greatest response (∼3 times greater than PD8 pups). Interestingly, the ACTH response to hypoxia was absent in PD2 pups, while plasma ACTH nearly tripled in PD8 pups. Analysis of adrenal mRNA expression revealed a hypoxia-induced increase in Ldlr mRNA at PD2, while both Ldlr and Star mRNA were increased at PD8. Acute hypoxia decreased arterial O2 saturation (SPo2) to ∼80% and also decreased body temperature by 5–6°C. The hypoxic thermal response may contribute to the ACTH and corticosterone response to decreases in oxygen. The present data describe a developmentally regulated, differential corticosterone response to acute hypoxia, shifting from ACTH independence in early life (PD2) to ACTH dependence less than 1 wk later (PD8).

Impaired glucagon secretion to insulin-induced hypoglycemia in anorexia nervosa

1989 ◽  
Vol 120 (5) ◽  
pp. 610-615 ◽  
Author(s):  
Shinichi Fujii ◽  
Hajime Tamai ◽  
Mitsuharu Kumai ◽  
Yukihiko Takaichi ◽  
Tetsuya Nakagawa ◽  
...  
Keyword(s):  
Anorexia Nervosa ◽  
Plasma Glucose ◽  
Cell Function ◽  
Insulin Response ◽  
Glucagon Secretion ◽  
Control Group ◽  
Arginine Infusion ◽  
Glucose Levels ◽  
Control Subjects ◽  
Glucose Recovery

Abstract. In order to clarify the role played by pancreatic α-cell dysfunction in the impaired glucose recovery from hypoglycemia in patients with anorexia nervosa, the response of pancreatic α-cells to insulin-induced hypoglycemia was investigated in 16 patients with anorexia nervosa before and after treatment. The results were compared with those obtained after loading with arginine. Before treatment, despite comparable falls in plasma glucose levels, glucagon secretion was significantly reduced in the anorectic patients compared with control subjects. In addition, glucose recovery from hypoglycemia in the patients was attenuated. However, after treatment, both glucagon secretory activity and plasma glucose recovery following insulin-induced hypoglycemia were restored to normal. Plasma glucagon responses to arginine infusion were not significantly different in the untreated anorectic patients and control subjects. However, the plasma insulin response in the patients was significantly lower than in the control group. These results suggest that the impaired recovery of plasma glucose levels from insulin-induced hypoglycemia in patients with anorexia nervosa is primarily attributable to impaired pancreatic α-secretory capability. In addition, this abnormality in pancreatic α-cell function is reversible with treatment leading to improved nutrition and weight gain.

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