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)

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.

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.

Glucose-Dependent Insulinotropic Polypeptide Is a Pancreatic Polypeptide Secretagogue in Humans

2019 ◽  
Vol 105 (3) ◽  
pp. e502-e510
Author(s):  
Simon Veedfald ◽  
Louise Vedtofte ◽  
Kirsa Skov-Jeppesen ◽  
Carolyn F Deacon ◽  
Bolette Hartmann ◽  
...  
Keyword(s):  
Pancreatic Polypeptide ◽  
Plasma Glucose ◽  
Exogenous Insulin ◽  
Healthy Individuals ◽  
Healthy Men ◽  
Glucose Levels ◽  
Fasting Glycemia ◽  
Islet Hormone ◽  
The Mean

Abstract Background Glucose-dependent insulinotropic polypeptide (GIP) has been suggested to stimulate the secretion of pancreatic polypeptide (PP), an islet hormone thought to regulate gut motility, appetite, and glycemia. Objective To determine whether human GIP1-42 (hGIP) stimulates PP secretion. Method As glycemia modulates the secretion of PP, we measured plasma PP concentrations from 2 studies in healthy men (n = 10) and in patients with type 2 diabetes (T2D) (n = 12), where hGIP1-42 had been administered intravenously during fasting glycemia, hyperglycemia (12 mmol/L), and insulin-induced hypoglycemia (targets: 2.5 mmol/L [healthy]; 3.5 mmol/L [T2D]). Porcine GIP1-42 (pGIP) was also infused intra-arterially in isolated porcine pancreata (n = 4). Results Mean fasting plasma glucose concentrations were approximately 5 mmol/L (healthy) and approximately 8 mmol/L (T2D). At fasting glycemia, PP concentrations were higher during intravenous hGIP1-42 infusion compared with saline in healthy men (mean [standard error of the mean, SEM], net incremental areas under the curves (iAUCs)[0-30min], 403 [116] vs –6 [57] pmol/L × min; P = 0.004) and in patients with T2D (905 [177] vs –96 [86] pmol/L × min; P = 0.009). During hyperglycemic clamping, mean [SEM] PP concentrations were significantly higher during hGIP1-42 infusion compared with saline in patients with T2D (771 [160] vs –183 [117] pmol/L × min; P = 0.001), but not in healthy individuals (–8 [86] vs –57 [53] pmol/L × min; P = 0.69). When plasma glucose levels were declining in response to exogenous insulin, mean [SEM] PP concentrations were higher during hGIP1-42 infusion compared with saline in healthy individuals (294 [88] vs –82 [53] pmol/L × min; P = 0.0025), but not significantly higher in patients with T2D (586 [314] vs –120 [53]; P = 0.070). At target hypoglycemia, PP levels surged in both groups during both hGIP1-42 and saline infusions. In isolated pancreata, pGIP1-42 increased mean [SEM] PP output in the pancreatic venous effluent (baseline vs infusion, 24[5] vs 79 [16] pmol/min x min; P = 0.044). Conclusion GIP1-42 increases plasma PP secretion in healthy individuals, patients with T2D, and isolated porcine pancreata. Hyperglycemia blunts the stimulatory effect of hGIP1-42 in healthy individuals, but not in patients with T2D.

The Effect of Glycemic Index on Plasma Glucose and Lactate Levels during Incremental Exercise

2000 ◽  
Vol 10 (1) ◽  
pp. 51-61 ◽  
Author(s):  
Stephen R. Stannard ◽  
Martin W. Thompson ◽  
Janette C. Brand Miller
Keyword(s):  
Glycemic Index ◽  
Plasma Glucose ◽  
Glucose Concentration ◽  
Lactate Concentration ◽  
Incremental Exercise ◽  
Plasma Glucose Concentration ◽  
Plasma Lactate ◽  
Significant Difference ◽  
Plasma Lactate Concentration ◽  
Lactate Levels

Consumption of low glycemic index (GI) foods before submaximal endurance exercise may be beneficial to performance. To test whether this may also be true for high intensity exercise. 10 trained cyclists began an incremental exercise test to exhaustion 65 min after consuming equal carbohydrate portions of glucose (HGI), pasta (LGI), and a noncarbohydrate control (PL). Time to fatigue did not differ significantly (p = 0.05) between treatments. Plasma glucose concentration was significantly lower after LGI vs. HGI from 15 to 45 min of rest postprandial. During exercise, plasma glucose concentration was significantly lower after HGI vs. LGI from 200 W until exhaustion. Plasma lactate concentration following HGI was significantly higher than PL from 30 min of rest postprandial through to the end of the 200-W workload. Plasma lactate concentration following LGI was significantly lower than after HGI from 45 min of rest postprandial through to the end of the 100-W workload. At higher exercise intensities, there was no significant difference in plasma lactate levels between treatments. These findings suggest that a high GI carbohydrate meal (1 g/kg body wt) 65 min prior to exercise decreases plasma glucose and increases plasma lactate levels compared to a low GI meal, but not enough to be detrimental to incremental exercise performance.

scholarly journals Assessment of Different Commercially Available Breads and Its Effect on Blood Glucose Levels of Healthy Individuals

2019 ◽  
pp. 1-5
Author(s):  
Bhavana Parmar ◽  
Rupali Sengupta
Keyword(s):  
Blood Glucose ◽  
Plasma Glucose ◽  
White Bread ◽  
Healthy Individuals ◽  
Glucose Response ◽  
High Blood Glucose ◽  
Glucose Levels ◽  
Blood Glucose Response ◽  
Blood Glucose Levels ◽  
Breakfast Food

Background: Bread is one of the most commonly used breakfast food in India. The consumption also increased tremendously among children and adolescents as well as to some extent among adults. It was found that white bread raises the blood glucose levels and is not considered to be a healthy breakfast option especially for those with diabetes mellitus and those at risk of increased or borderline glucose intolerance. Aim: To assess different commercially available bread and its effect on Blood Glucose Levels of Healthy Individuals. Study Design: 5 bread varieties were chosen (namely White, Brown, Multigrain, Oats and Tutty fruity bread). The samples were fed to 30 subjects and their effect on blood glucose was analysed. Place of Study: The study was conducted in BMN College of Home Science, Matunga, Mumbai, India. Methodology: A pilot study was conducted on 30 samples to assess the Blood Glucose Levels of each type of bread. The subjects were then given bread-butter and the blood glucose response was re-tested at gap of 1 hour and 2 hour respectively. Each subject was given 5 different varieties of bread for 5 consecutive days i.e. White bread, Brown bread, Multigrain bread, Tutty Fruity bread and Oats bread. White bread is a universal standard, was used as a standard in the study.  The average plasma glucose levels were analysed in the study. Results: The average plasma glucose spike of the standard (White bread) was found to be the highest i.e (131.63 mg/dl).  It was observed that oats bread was found to have the lowest spike post 1 hour (103.43mg/dl) while tutty fruity bread exhibited a very high blood glucose response (123.90mg/dl) following the standard white bread. Conclusion: Investigations proved that oats bread should be consumed by people to mitigate metabolic syndrome due to a stressful lifestyle. Also, a healthy diet and exercise regime to be followed by subjects in the study.

scholarly journals Type-2-diabetes Alters CSF but not Plasma Metabolomic and AD Risk Profiles in Vervet Monkeys

2019 ◽  
Author(s):  
Kylie Kavanagh ◽  
Stephen M. Day ◽  
Morgan C. Pait ◽  
William R. Mortiz ◽  
Christopher B. Newgard ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Amino Acids ◽  
Cerebral Metabolism ◽  
Vervet Monkeys ◽  
Plasma Lactate ◽  
Glucose Levels ◽  
Highly Correlated ◽  
Lactate Levels ◽  
The Brain

AbstractEpidemiological studies suggest that individuals with type 2 diabetes (T2D) have a 2-4 fold increased risk for developing Alzheimer’s disease (AD), however the exact mechanisms linking the two disease is unknown. In both conditions, the majority of pathophysiological changes (including glucose and insulin dysregulation, insulin resistance, and AD-related changes in Aβ and tau) occur decades before the onset of clinical symptoms and diagnosis. In this study, we investigated the relationship between metabolic biomarkers associated with T2D and AD-related pathology, including Aβ levels, from cerebrospinal fluid (CSF) and fasting plasma of healthy, prediabetic (PreD), and T2D vervet monkeys (Chlorocebus aethiops sabeus). Consistent with the human disease, T2D monkeys have increased plasma and CSF glucose levels as they transition from normoglycemia to pre-diabetic and diabetic states. Although plasma levels of acylcarnitines and amino acids remained largely unchanged, peripheral hyperglycemia correlated with decreased CSF acylcarnitines and CSF amino acids, including branched chain amino acid (BCAA) concentrations, suggesting profound changes in cerebral metabolism coincident with systemic glucose dysregulation. Moreover, CSF Aβ40 and CSF Aβ42 levels decreased in T2D monkeys, a phenomenon observed in the human course of AD which coincides with increased amyloid deposition within the brain. In agreement with our previous studies in mice, CSF Aβ40 and CSF Aβ42 were highly correlated with CSF glucose levels, suggesting that glucose levels in the brain are associated with changes in Aβ metabolism. Interestingly, CSF Aβ40 and CSF Aβ42 levels were also highly correlated with plasma but not CSF lactate levels, suggesting that plasma lactate might serve as a potential biomarker of disease progression in AD. Moreover, CSF glucose and plasma lactate levels were correlated with CSF amino acid and acylcarnitine levels, demonstrating alterations in cerebral metabolism occurring with the onset of T2D. Together, these data suggest that peripheral metabolic changes associated with the development of T2D produce alterations in brain metabolism that lead to early changes in the amyloid cascade, similar to those observed in pre-symptomatic AD.

Metabolic and physiological response of the rabbit to continuous and intermittent treadmill exercise

1990 ◽  
Vol 68 (7) ◽  
pp. 856-862 ◽  
Author(s):  
H. Meng ◽  
G. N. Pierce
Keyword(s):  
Animal Model ◽  
Intermittent Exercise ◽  
Vastus Lateralis ◽  
Plasma Triglyceride ◽  
Treadmill Running ◽  
Vastus Lateralis Muscle ◽  
Plasma Lactate ◽  
Glucose Levels ◽  
High Speeds ◽  
Lactate Levels

Our knowledge of the effects of exercise on the heart is limited by the predominant use of rats as an animal model. The rabbit has many advantages over the rat as an animal model to study. However, little work has characterized its capacity to exercise. The purposes of the present study were to determine if the rabbit could (i) learn to run on a motor-driven treadmill at relatively high speeds using different exercise protocols, and (ii) characterize the various physiological and metabolic responses of the rabbit to acute bouts of exercise. We found that female New Zealand white rabbits had the capacity to run continuously on the treadmill for up to 21 min at 20 m/min until exhausted. Continuous, endurance-type exercise resulted in significant elevations in body temperature, heart rate, and plasma lactate levels. Plasma triglyceride concentration decreased as a function of this type of running whereas plasma glucose levels were unchanged. Twenty-four hours after a bout of running, plasma creatine phosphokinase activity was significantly elevated. The rabbits also had the capacity to learn to run using an intermittent, higher speed protocol. These physically untrained animals could achieve speeds of up to 70 m/min for 10 bouts of 15 s run/30 s rest. Their metabolic and physiological responses to this protocol were similar to those of continuous running with the following exceptions. The decrease in plasma triglyceride was less marked and the increase in plasma lactate was greater after intermittent exercise. Glycogen content of the rabbit vastus lateralis muscle was also significantly depleted after exhaustive, intermittent exercise. Our results demonstrate that rabbits can learn to run using different exercise protocols on a treadmill and, therefore, could serve as an appropriate model in which to study exercise conditioning. Their ability to run at extremely high speeds and withstand relatively intense exercise bouts will be particularly useful in future investigations of the cardiovascular adaptations of the rabbit to exercise training.Key words: exercise, rabbit, treadmill running, lactate, glycogen.

Important role of glucagon during exercise in diabetic dogs

1985 ◽  
Vol 59 (4) ◽  
pp. 1272-1281 ◽  
Author(s):  
D. H. Wasserman ◽  
H. L. Lickley ◽  
M. Vranic
Keyword(s):  
Plasma Glucose ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Immunoreactive Insulin ◽  
Metabolic Clearance ◽  
Glucose Levels ◽  
Lower Glucose ◽  
Diabetic Dogs ◽  
Lactate Levels

To define the role of immunoreactive glucagon (IRG) during exercise in diabetes, 12 insulin-deprived alloxan-diabetic (A-D) dogs were run for 90 min (100 m/min, 12 degrees) with or without somatostatin (St 0.5 microgram . kg-1 . min-1). Compared with normal dogs, A-D dogs were characterized by similar hepatic glucose production (Ra), lower glucose metabolic clearance, and higher plasma glucose and free fatty acid levels during rest and exercise. In A-D dogs IRG was greater at rest and exhibited a threefold greater exercise increment than controls, whereas immunoreactive insulin (IRI) was reduced by 68% at rest but had similar values to controls during exercise. Basal norepinephrine, epinephrine, cortisol, and lactate levels were similar in normal and A-D dogs. However, exercise increments in norepinephrine, cortisol, and lactate were higher in A-D dogs. When St was infused during exercise in the A-D dogs, IRG was suppressed by 432 +/- 146 pg/ml below basal and far below the exercise response in A-D controls (delta = 645 +/- 153 pg/ml). IRI was reduced by 1.8 +/- 0.2 microU/ml with St. With IRG suppression the increase in Ra seen in exercising A-D controls (delta = 4.8 +/- 1.6 mg . kg-1 . min-1) was virtually abolished, and glycemia fell by 104 to 133 +/- 37 mg/dl. Owing to this decrease in glycemia, the increase in glucose disappearance was attenuated. Despite the large fall in glucose during IRG suppression, counterregulatory increases were not excessive compared with A-D controls. In fact, as glucose levels approached euglycemia, the increments in norepinephrine and cortisol were reduced to levels similar to those seen in normal exercising dogs. In conclusion, IRG suppression during exercise in A-D dogs almost completely obviated the increase in Ra, resulting in a large decrease in plasma glucose. Despite this large fall in glucose, there was no excess counterregulation, since glucose concentrations never reached the hypoglycemic range.

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