Effects of Acute Exposure to Bleached Kraft Pulpmill Effluent on Carbohydrate Metabolism of Juvenile Coho Salmon (Oncorhynchus kisutch) During Rest and Exercise

1975 ◽  
Vol 32 (6) ◽  
pp. 753-760 ◽  
Author(s):  
D. J. McLeay ◽  
D. A. Brown
Keyword(s):  
Plasma Glucose ◽  
Muscle Glycogen ◽  
Coho Salmon ◽  
Liver Glycogen ◽  
Plasma Lactate ◽  
Mean Values ◽  
Glucose Levels ◽  
Lactate Levels ◽  
Sugar Levels ◽  
Glycogen Stores

In the static study (no exercise), liver glycogen stores were unchanged during 12-h exposure to 0.8 of the 96-h LC50; longer exposures caused a progressive decrease to levels one fifth those of controls at 72 h. Plasma glucose levels in fish held in 0.8 LC50 effluent for 3–96 h were elevated; at 96 h, glucose had increased threefold. Mean values for plasma lactate were elevated significantly at 3, 6, 24, 72, and 96 h.In the exercise (swimming one body length per second)–rest study, muscle glycogen levels decreased 53–78% during exercise in water or effluent (0.7 LC50) for 4–12 h, and did not recover during 12-h rest in water. Muscle glycogen for fish exercised for 12 h in effluent and then rested for 4 or 12 h in effluent was lower compared to values for fish exercised in effluent and then rested in water. There was no difference in liver glycogen levels offish exercised in effluent or water for 4–12 h. Values of liver glycogen for fish exercised in effluent for 12 h and then rested for 4, 8, or 12 h in effluent decreased 60–70% compared to fish exercised in water for 12 h and then rested in water and by 55–65% from fish exercised in effluent for 12 h and rested in water for 4–12 h. Plasma glucose levels were elevated one- to fourfold during exercise in water or effluent. Fish resting in water for 4, 8, or 12 h following exercise in water had relatively stable glucose levels; whereas for fish exercised and then rested in effluent the glucose levels increased twofold during resting. Plasma lactate levels were elevated five- to sixfold during exercise in water or effluent for 4–12 h, declining to values 1–2 times those of stock fish within 4-h rest. Plasma lactate levels for fish exercised in effluent and then rested in effluent or water were continually higher than those for fish exercised and rested in water.It was concluded that measurement of carbohydrate metabolites, particularly blood sugar levels, in unexercised fish could prove useful as a rapid method for measuring toxicity of pulpmill effluents and other pollutants.

Development of a Blood Sugar Bioassay for Rapidly Measuring Stressful Levels of Pulpmill Effluent to Salmonid Fish

1977 ◽  
Vol 34 (4) ◽  
pp. 477-485 ◽  
Author(s):  
Donald J. McLeay
Keyword(s):  
Blood Sugar ◽  
Plasma Glucose ◽  
Coho Salmon ◽  
Rapid Test ◽  
Liver Glycogen ◽  
Threshold Effect ◽  
Salmo Gairdneri ◽  
Glucose Levels ◽  
Sugar Levels ◽  
Effluent Exposure

The hyperglycemic stress response of fish was evaluated for use as a rapid test for assessing stressful levels of pulpmill effluents (BKME). Plasma glucose levels in juvenile coho salmon (Oncorhynchus kisutch) were elevated within 0.5 h following transfer from the holding tank to aquaria containing either fresh water or BKME, peaking at 3–6 h and returning to near-basal levels at 24 h. Acclimation of coho to aquaria for 24, 48, 72, or 96 h prior to addition of effluent resulted in marked increases in glucose levels attributable to BKME. Significant responses to effluent were found with exposures of 3–10 h, whereas levels were not increased with exposures of 2 h or less. Plasma glucose levels increased progressively with increasing effluent concentrations. Threshold effect (EC50) values varied from 0.04 to 0.16 of the 96-h LC50 values. The response to BKME treated previously by the activated sludge process or by foam separation was diminished or absent altogether.Juvenile rainbow trout (Salmo gairdneri) and coho displayed a hyperglycemic response with 4-, 6-, or 8-h exposure to an identical effluent concentration, although the magnitude of response of rainbow was less in each instance.The extent to which blood sugar levels are elevated due to effluent exposure is directly related to the liver glycogen reserves of the fish. Acclimation to test tanks for 24–48 h followed by exposure for 3–6 h is suggested as the best working combination for this test.

Response to intravenous injections of amylin and glucagon in fasted, fed, and hypoglycemic rats

1993 ◽  
Vol 264 (6) ◽  
pp. E943-E950 ◽  
Author(s):  
A. A. Young ◽  
G. J. Cooper ◽  
P. Carlo ◽  
T. J. Rink ◽  
M. W. Wang
Keyword(s):  
Plasma Glucose ◽  
Insulin Infusion ◽  
Sodium Lactate ◽  
Plasma Lactate ◽  
Glucose Response ◽  
Intravenous Injections ◽  
Glucose Levels ◽  
Fasted State ◽  
Islet Hormone ◽  
Lactate Levels

The actions of intravenous glucagon and amylin, a newly discovered hyperglycemic pancreatic islet hormone, have been compared in 20-h fasted and fed, lightly anesthetized rats, and in rats made hypoglycemic with an insulin infusion. In fasted animals, amylin (75 nmol/kg) was more effective than glucagon (90 nmol/kg) in increasing plasma glucose (glucose increment 4.55 vs. 1.71 mM, P < 0.001). Amylin elicited a marked increase in plasma lactate, as previously reported, whereas glucagon did not alter plasma lactate. In fed animals, glucagon elicited twice as much increase in plasma glucose as did amylin; amylin again elicited a marked lactate increase that was greater (increment 1.45 vs. 0.97 mM, P < 0.05) and more prolonged than in the fasted state, whereas glucagon was without effect on lactate levels. These findings are consistent with glucagon's known action to promote hyperglycemia from hepatic glycogenolysis and amylin's demonstrated action to promote muscle glycogenolysis and increase lactate supply to the liver. Infusions of sodium lactate that produced plasma lactate increments similar to those evoked by 75 nmol/kg amylin evoked patterns of glucose response in fasted and fed rats similar to those evoked by amylin. Thus increased lactate supply to the liver may account for amylin's hyperglycemic effects. Amylin and glucagon could each restore plasma glucose to control levels in fasted animals made hypoglycemic by insulin infusion (plasma glucose reduced to 3.3 mM). A bolus of 75 nmol/kg amylin was more effective than 180 nmol/kg glucagon, restoring basal glucose levels for > 3 h, whereas glucagon restored it for < 1 h.(ABSTRACT TRUNCATED AT 250 WORDS)

Glucose turnover in 48-hour-fasted running rats

1987 ◽  
Vol 252 (3) ◽  
pp. R587-R593 ◽  
Author(s):  
B. Sonne ◽  
K. J. Mikines ◽  
H. Galbo
Keyword(s):  
Plasma Glucose ◽  
Muscle Glycogen ◽  
Lactate Production ◽  
Glucose Production ◽  
Liver Glycogen ◽  
Glucose Turnover ◽  
Feedback Mechanisms ◽  
Glycogen Stores ◽  
Resting Muscle ◽  
Fasted Rats

In fed rats, hyperglycemia develops during exercise. This contrasts with the view based on studies of fasted human and dog that euglycemia is maintained in exercise and glucose production (Ra) controlled by feedback mechanisms. Forty-eight-hour-fasted rats (F) were compared to fed rats (C) and overnight food-restricted (FR) rats. [3-3H]- and [U-14C] glucose were infused and blood and tissue sampled. During running (21 m/min, 0% grade) Ra increased most in C and least in F and only in F did Ra not significantly exceed glucose disappearance. Plasma glucose increased more in C (3.3 mmol/l) than in FR (1.6 mmol/l) and only modestly (0.6 mmol/l) and transiently in F. Resting liver glycogen and exercise glycogenolysis were highest in C and similar in FR and F. Resting muscle glycogen and exercise glycogenolysis were highest in C and lowest in F. During running, lactate production and gluconeogenesis were higher in FR than in F. At least in rats, responses of production and plasma concentration of glucose to exercise depend on size of liver and muscle glycogen stores; glucose production matches increase in clearance better in fasted than in fed states. Probably glucose production is stimulated by “feedforward” mechanisms and “feedback” mechanisms are added if plasma glucose decreases.

Gluconeogenic pathway in liver and muscle glycogen synthesis after exercise

1988 ◽  
Vol 64 (4) ◽  
pp. 1591-1599 ◽  
Author(s):  
J. L. Johnson ◽  
G. J. Bagby
Keyword(s):  
Plasma Glucose ◽  
Muscle Glycogen ◽  
White Muscle ◽  
Glycogen Synthesis ◽  
Plasma Lactate ◽  
Indirect Pathway ◽  
Direct Pathway ◽  
Prior Exercise ◽  
Muscle Glycogen Synthesis ◽  
Lactate Levels

To determine whether prior exercise affects the pathways of liver and muscle glycogen synthesis, rested and postexercised rats fasted for 24 h were infused with glucose (200 mumol.min-1.kg-1 iv) containing [6-3H]glucose. Hyperglycemia was exaggerated in postexercised rats, but blood lactate levels were lower than in nonexercised rats. The percent of hepatic glycogen synthesized from the indirect pathway (via gluconeogenesis) did not differ between exercised (39%) and nonexercised (36%) rats. In red muscle, glycogen was synthesized entirely by the direct pathway (uptake and phosphorylation of plasma glucose) in both groups. However, only approximately 50% of glycogen was formed via the direct pathway in white muscle of exercised and nonexercised rats. Therefore prior exercise did not alter the pathways of tissue glycogen synthesis. To further study the incorporation of gluconeogenic precursors into muscle glycogen, exercised rats were infused with either saline, lactate (100 mumol.min-1.kg-1), or glucose (200 mumol.min-1.kg-1), containing [6-3H]glucose and [14C(U)]lactate. Plasma glucose was elevated one- to twofold and three- to fourfold by lactate and glucose infusion, respectively. Plasma lactate levels were elevated by about threefold during both glucose and lactate infusion. Glycogen was partially synthesized via an indirect pathway in white muscle and liver of glucose- or lactate-infused rats but not in saline-infused animals. Thus participation of an indirect pathway in white skeletal muscle glycogen synthesis required prolonged elevation of plasma lactate levels produced by nutritive support.

Cortisol-induced changes in plasma glucose, protein, and thyroid hormone levels, and liver glycogen content of coho salmon (Oncorhynchus kisutch Walbaum)

1989 ◽  
Vol 67 (11) ◽  
pp. 2746-2750 ◽  
Author(s):  
M. M. Vijayan ◽  
J. F. Leatherland
Keyword(s):  
Plasma Glucose ◽  
Plasma Cortisol ◽  
Glycogen Content ◽  
Coho Salmon ◽  
Coconut Oil ◽  
Liver Glycogen ◽  
Hepatosomatic Index ◽  
Glucose Levels ◽  
Liver Glycogen Content ◽  
Cortisol Levels

Coho salmon given intraperitoneal implants of hydrogenated coconut oil alone or coconut oil containing cortisol at 1, 5, or 10 mg/fish exhibited dose-related increases in plasma cortisol levels at day 15. After 30 days, plasma cortisol levels were significantly higher in the cortisol-implanted groups but there was no dose-related response. Plasma T3 levels were lowered in cortisol-treated fish, but plasma T4 levels were not consistently affected. Plasma glucose levels were significantly higher in the group treated with cortisol at 10 mg/fish than in the controls on both sampling days, whereas liver glycogen content and hepatosomatic index were significantly lower in the cortisol-treated groups at day 30 but not at day 15. Plasma protein levels were not significantly different between treatments at either sampling time. The splenosomatic indices were not significantly different in the three treatment groups at day 15, but at day 30 the values in the 5 and 10 mg/fish cortisol-treated groups were significantly higher than in the controls.

scholarly journals Gluconeogenesis from lactate in the developing rat. Studies in vivo

1972 ◽  
Vol 127 (3) ◽  
pp. 531-537 ◽  
Author(s):  
Richard G. Vernon ◽  
Deryck G. Walker
Keyword(s):  
Skeletal Muscle ◽  
Plasma Glucose ◽  
Muscle Glycogen ◽  
Half Life ◽  
Specific Radioactivity ◽  
Liver Glycogen ◽  
Plasma Lactate ◽  
Old Rats ◽  
Developing Rat

1. The specific radioactivity of plasma l-lactate and the incorporation of 14C into plasma d-glucose, liver glycogen and skeletal-muscle glycogen were measured as a function of time after the intraperitoneal injection of l-[U-14C]lactate into 2-, 10- and 30-day-old rats. 2. Between 15 and 60min after the injection of the l-[U-14C]lactate, the specific radioactivity of plasma lactate decreased with a half-life of 20–33min in animals at all three ages. 3. At all times after injection examined, the specific radioactivity of plasma glucose of the 2- and 10-day-old rats was at least fourfold greater than that of the 30-day-old rats. 4. Although 14C was incorporated into liver glycogen the amount incorporated was always less than 5% of that present in plasma glucose. 5. The results are discussed with reference to the factors that may influence the rate of incorporation of 14C into plasma glucose, and it is concluded that the rate of gluconeogenesis in the 2- and 10-day-old suckling rat is at least twice that of the weaned 30-day-old animal.

scholarly journals Examination of Potential Mechanisms in the Enhancement of Cerebral Blood Flow by Hypoglycemia and Pharmacological Doses of Deoxyglucose

1997 ◽  
Vol 17 (1) ◽  
pp. 54-63 ◽  
Author(s):  
Naoaki Horinaka ◽  
Nicole Artz ◽  
Jane Jehle ◽  
Shinichi Takahashi ◽  
Charles Kennedy ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Glucose Metabolism ◽  
Plasma Glucose ◽  
Plasma Lactate ◽  
Insulin Hypoglycemia ◽  
Glucose Levels ◽  
Arterial Blood ◽  
Arterial Plasma

Cerebral blood flow (CBF) rises when the glucose supply to the brain is limited by hypoglycemia or glucose metabolism is inhibited by pharmacological doses of 2-deoxyglucose (DG). The present studies in unanesthetized rats with insulin-induced hypoglycemia show that the increases in CBF, measured with the [14C]iodoantipyrine method, are relatively small until arterial plasma glucose levels fall to 2.5 to 3.0 m M, at which point CBF rises sharply. A direct effect of insulin on CBF was excluded; insulin administered under euglycemic conditions maintained by glucose injections had no effects on CBF. Insulin administration raised plasma lactate levels and decreased plasma K+ and HCO3– concentrations and arterial pH. These could not, however, be related to the increased CBF because insulin under euglycemic conditions had similar effects without affecting CBF; furthermore, the inhibition of brain glucose metabolism with pharmacological doses (200 mg/kg intravenously) of DG increased CBF, just like insulin hypoglycemia, without altering plasma lactate and K+ levels and arterial blood gas tensions and pH. Nitric oxide also does not appear to mediate the increases in CBF. Chronic blockade of nitric oxide synthase activity by twice daily i.p. injections of NG-nitro-L-arginine methyl ester for 4 days or acutely by a single i.v. injection raised arterial blood pressure and lowered CBF in normoglycemic, hypoglycemic, and DG-treated rats but did not significantly reduce the increases in CBF due to insulin-induced hypoglycemia (arterial plasma glucose levels, 2.5-3 m M) or pharmacological doses of deoxyglucose.

Regulation of hepatic gluconeogenesis and glycogenolysis by catecholamines in rainbow trout during environmental hypoxia

1989 ◽  
Vol 147 (1) ◽  
pp. 169-188 ◽  
Author(s):  
P. A. Wright ◽  
S. F. Perry ◽  
T. W. Moon
Keyword(s):  
Rainbow Trout ◽  
Plasma Glucose ◽  
Glycogen Phosphorylase ◽  
Active Form ◽  
Glucose Levels ◽  
Mediated Effects ◽  
Inhibition Of Glycolysis ◽  
Pre Treatment ◽  
Lactate Levels ◽  
Liver Glycogenolysis

This study tests the hypothesis that catecholamines regulate glucose availability during hypoxia in the rainbow trout by activating glycogen phosphorylase (GPase) while inhibiting pyruvate kinase (PK) in the liver. The net result would be an increase in liver glycogenolysis and a reduction of glycolysis and/or enhancement of gluconeogenesis. We used the criteria of Stalmans & Hers (1975) and report much lower resting percent GPase a (active) values (20–30%) than those previously published. Dorsal aortic injections of epinephrine or norepinephrine increased plasma glucose (16–46%), had no effect on liver or muscle glycogen levels, decreased the activity of PK, and increased total and percent GPase a activities. Pre-treatment with the beta-adrenoreceptor antagonist propranolol eliminated these effects. During moderate hypoxia, plasma glucose remained unchanged, while lactate levels increased fourfold. When fish were pre-treated with propranolol, hypoxia depressed plasma glucose levels (−26%), total and percent GPase a, and increased PK activity, suggesting that hypoxia mediated the dephosphorylation of these enzymes. We conclude that catecholamines stimulate hepatic beta-adrenoreceptors during hypoxia and sustain plasma glucose levels by nullifying the deleterious effects of hypoxia on metabolic function. The specific metabolic consequences of these catecholamine-mediated effects are an increase in the activity of the active form of GPase and a reduction in PK activity, which suggests an activation of glycogenolysis and an inhibition of glycolysis and/or activation of gluconeogenesis, respectively.

VARIATIONS IN GLUCAGON RESPONSE AMONG JUVENILE DIABETICS

PEDIATRICS ◽  
1963 ◽  
Vol 32 (6) ◽  
pp. 1002-1006
Author(s):  
Donnell D. Etzwiler
Keyword(s):  
Blood Glucose ◽  
Good Control ◽  
Liver Glycogen ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Juvenile Diabetics ◽  
Glycogen Stores ◽  
Initial Blood ◽  
Hyperglycemic Effect

Glucagon or a placebo preparation was administered to 65 juvenile diabetics on 74 separate occasions. When the initial blood glucose of these children showed them to be in reasonably good control, glucagon produced a hyperglycemic effect. However, when the blood glucose levels were markedly elevated, the effect of glucagon was less predictable. The depletion of liver glycogen stores and the possible effect of contaminating insulin in glucagon preparations are discussed.

Maternal ethanol ingestion: effect on maternal and neonatal glucose balance

1986 ◽  
Vol 251 (2) ◽  
pp. E178-E184 ◽  
Author(s):  
L. Witek-Janusek
Keyword(s):  
Liver Glycogen ◽  
Maternal Plasma ◽  
Postnatal Period ◽  
Female Rats ◽  
Ethanol Ingestion ◽  
Chow Diet ◽  
Fed State ◽  
Glucose Levels ◽  
Rat Pups ◽  
Glycogen Stores

Liver glycogen availability in the newborn is of major importance for the maintenance of postnatal blood glucose levels. This study examined the effect of maternal ethanol ingestion on maternal and neonatal glucose balance in the rat. Female rats were placed on the Lieber-DeCarli liquid ethanol diet, an isocaloric liquid pair-fed diet, or an ad libitum rat chow diet at 3 wk before mating and throughout gestation. Blood and livers were obtained from dams and rat pups on gestational days 21 and 22. The pups were studied up to 6 h in the fasted state and up to 24 h in the fed state. Maternal ethanol ingestion significantly decreased litter size, birth weight, and growth. A significantly higher mortality during the early postnatal period was seen in the prenatal ethanol exposed pups. Ethanol significantly decreased fed maternal liver glycogen stores but not maternal plasma glucose levels. The newborn rats from ethanol ingesting dams also had significantly decreased liver glycogen stores. Despite mobilizing their available glycogen, these prenatal ethanol exposed pups became hypoglycemic by 6 h postnatal. This was more marked in the fasted pups. Ethanol did not affect maternal nor neonatal plasma insulin levels. Thus maternal ethanol ingestion reduces maternal and neonatal liver glycogen stores and leads to postnatal hypoglycemia in the newborn rat.

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