Glucose turnover in the post-absorptive rat and the effects of halothane anaesthesia

Heath, D. F.; Frayn, Keith N.; Rose, Jonathan A.

doi:10.1042/bj1620653

Cited by 18 publications

(3 citation statements)

References 20 publications

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“…Then, during suckling glucagon stimulation ensures hepatic synthesis of glucose, which is otherwise poorly provided by mother's milk (18). Similarly, during starvation in adults glucose produced by the liver is the main energy source utilized by splanchnic tissues and brain (19). In pathological situations such as diabetes, elevated hepatic glucose production is one of the key features responsible for hyperglycemia (20).…”

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confidence: 99%

In Vivo and in Vitro Regulation of Hepatic Glucagon Receptor mRNA Concentration by Glucose Metabolism

Burcelin¹,

Mrejen²,

Decaux³

et al. 1998

Journal of Biological Chemistry

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We have recently cloned the murine glucagon receptor (GR) gene and shown that it is expressed mainly in liver. In this organ, the glucagon-GR system is involved in the control of glucose metabolism as it initiates a cascade of events leading to release of glucose into the blood stream, which is a main feature in several physiological and pathological conditions. To better define the metabolic regulators of GR expression in liver we analyzed GR mRNA concentration in physiological conditions associating various glucose metabolic pathways in vivo and in vitro in the rat and in the mouse. First, we report that the concentration of the GR mRNA progressively increased from the first day of life to the adult stage. This effect was abolished when newborn rodents were fasted. Second, under conditions where intrahepatic glucose metabolism was active such as during fasting, diabetes, and hyperglycemic clamp, the concentration of GR mRNA increased independent of the origin of the pathway that generated the glucose flux. These effects were blunted when hyperglycemia was corrected by phlorizin treatment of diabetic rats or not sustained during euglycemic clamp.In accordance with these observations, we demonstrated that the glycolytic substrates glucose, mannose, and fructose, as well as the gluconeognic substrates glycerol and dihydroxyacetone, increased the concentration of GR mRNA in primary cultures of hepatocytes from fed rats. Glucagon blunted the effect of glucose without being dominant. The stimulatory effect of those substrates was not mimicked by the nonmetabolizable carbohydrate L-glucose or the glucokinase inhibitor glucosamine or when hepatocytes were isolated from starved rats. In addition, inhibitors of gluconeogenesis and lipolysis could decrease the concentration of GR mRNA from hepatocytes of starved rats. Combined, these data strongly suggest that glucose flux in the glycolytic and gluconeogenic pathways at the level of triose intermediates could control expression of GR mRNA and participate in controlling its own metabolism. The glucagon receptor (GR)1 is a 63,000-Da plasma membrane protein that belongs to a subfamily of peptide hormone receptors (1, 2). All members of this family contain seven transmembrane domains and are coupled with GTP-binding proteins. Upon binding to its receptor, glucagon initiates its action by activating several GTP-binding proteins which are ratelimiting steps in various signal transduction cascades (3-12).The GR gene is expressed mainly in liver (2,8,13,14) where it initiates a cascade of events leading to synthesis and release of glucose into the blood stream (15). Hepatic glucose production represents a major process in several physiological and pathological conditions. In newborns, glucagon is secreted within an hour of parturition and initiates several processes leading to hepatic glucose production (16) from glycogenolysis and gluconeogenesis (17). Then, during suckling glucagon stimulation ensures hepatic synthesis of glucose, which is otherwise poorly provided by mother's...

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confidence: 99%

In Vivo and in Vitro Regulation of Hepatic Glucagon Receptor mRNA Concentration by Glucose Metabolism

Burcelin¹,

Mrejen²,

Decaux³

et al. 1998

Journal of Biological Chemistry

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“…Previous studies showed minimal increases in blood glucose levels with halothane in fed rats (17), and with isofl urane in fed dogs (18). However, in another study, authors showed signifi cant increases in the blood glucose levels for a 3 hr period in fed rats when compared to blood glucose levels determined in fasted rats (200 mg/dl versus 130 mg/dl).…”

Section: Discussionmentioning

confidence: 78%

Are there any effects of Sevoflurane and Desflurane anaesthesia on blood glucose levels in acute hyperglycemic diabetic rats?

Dikmen¹,

Arpacı²,

Kalaycı³

et al. 2016

BLL

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AIM: The aim of this study was to investigate blood glucose level of desfl urane and sevofl urane on blood glucose in diabetic rats undergoing acute hyperglycemia. MATERIALS AND METHODS: In this study, 30 male Wistar albino rats were included. Diabetes was induced by a single IP injection of streptozotocin. After the effects of chronic diabetes encountered, diabetic rats were randomly assigned into diabetic control (group DC), diabetic hyperglycemia group (group DH), diabetic hyperglycemia group with desfl urane (group DH-D), and diabetic hyperglycemia group with sevofl urane (group DH-S) groups. The normoglycemic groups received an IP injection of the same amount of saline. Hyperglycemic diabetic rats were anaesthetized by desfl urane 6 % or sevofl urane 2 % at a dose, by which minimal alveolar concentration (MAC) for rats would be one. The drugs were given for 4 hours within 100 % oxygen at a rate of 6 L.min -1 . One hour after cessation of inhalation anesthesia, blood glucose levels were determined at 1st, 4th and 24th hours. 24 hours after the anaesthesia. RESULTS: Serum glucose was detected to be signifi cantly lower in Group C, when compared to Groups DC, DH, DH-D and DH-S (p = 0.002, p = 0.001, p = 0.002, p = 0.003, respectively). Blood glucose levels in the diabetic groups were similar at the end of 6 weeks period, after hyperglycemia and anaesthesia induction. CONCLUSION: We found out that sevofl urane and desfl urane administrations in hyperglycemic rats were both related with insignifi cant blood glucose level increase at early post anaesthesia period and at post anaesthesia 24th hours. We still think that patients undergoing anaesthesia protocols with acute hyperglycemia need relatively longer follow up periods (Tab. 1, Ref. 28). Text in PDF www.elis.sk.

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“…In contrast, the experimental rats received a solution of 15% glucose at the same rate. After 5 hours of infusion the glucose turnover rate was determined by a single injection tracer technique (Heath, Frayn and Rose 1977), in the awake post-absorptive rats. Plasma glucose and insulin concentration and glucose specific activity was measured as previously described ?…”

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confidence: 99%

Glucose Kinetics in the Chronically Hyperinsulinemic Rat

Arnow¹,

Jb²,

Schwartz³

1982

Horm Metab Res

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Glucose turnover in the post-absorptive rat and the effects of halothane anaesthesia

Cited by 18 publications

References 20 publications

In Vivo and in Vitro Regulation of Hepatic Glucagon Receptor mRNA Concentration by Glucose Metabolism

In Vivo and in Vitro Regulation of Hepatic Glucagon Receptor mRNA Concentration by Glucose Metabolism

Are there any effects of Sevoflurane and Desflurane anaesthesia on blood glucose levels in acute hyperglycemic diabetic rats?

Glucose Kinetics in the Chronically Hyperinsulinemic Rat

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