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Available data showed that the intestine increases it glucose uptake in response to hyperglycemia induced by anycause. However, what the intestine does with the glucose is not known. This study investigated the metabolic fate of theglucose taken up by the intestine during hyperglycaemia in dogs. Experiments were carried out on fasted, male, anaesthetizedmongrel dogs divided into 4 groups. The control (group 1, n=5) received normal saline (0.2 ml/kg) while groups 2-4(subdivided into two as low or high dose, n=5 each) received adrenaline (1 μg/kg or 5 μg/kg), glucagon (3 ng/kg or 8 ng/kg)and glucose (10 mg/kg/min or 20 mg/kg/min). Through a midline laparatomy, the upper jejunum was cannulated for IntestinalBlood Flow (IBF) measurement. Blood glucose and lactate levels were determined using glucose oxidase and lactatedehydrogenase methods, respectively. Intestinal Glucose/Lactate Uptake (IGU/ILU) was calculated as the product of IBFand arterio-venous glucose /lactate difference [(A-V) glucose/lactate]. Jejunal tissue samples were obtained for the determinationof Glycogen Content (GC) and activities of Glycogen Synthase (GS), Glycogen Phosphorylase 'a' (GPa), hexokinase andglucose-6-phosphatase. Anthrone method was used to determine GC while activities of GS, GPa, hexokinase and glucose-6-phosphatase were determined spectrophotometrically. Data were subjected to descriptive statistics and analyzed usingstudent's t-test and ANOVA at α0.05. Arterial and venous blood glucose and lactate were increased by adrenaline, glucagonand glucose. Venous lactate was higher than arterial lactate in all groups. Intestinal blood flow, (A-V) glucose and (A-V)lactate were increased in all the experimental groups. Intestinal glucose uptake increased by 624% (adrenaline), 705%(glucagon) and 589% (glucose) while intestinal lactate release increased by 422%, 459% and 272% respectively. IntestinalGC increased from 138.72 ± 4.58 mg/100 g to 167.17 ± 4.20 mg/100 g (adrenaline), 229.21 ± 6.25 mg/100 g (glucagon) and165.17 ± 4.20 mg/100 g (glucose). Adrenaline and glucose had no effect on GS activity but it was increased by glucagon;GPa was decreased while hexokinase activity was increased by adrenaline, glucagon, and glucose. Glucose-6-phosphataseactivity was not affected by adrenaline and glucagon but decreased by glucose. The intestine modulates blood glucose levelsthrough lactate formation, glycogen formation and most probably conversion of lactate to glucose through gluconeogenesis.
This article was published in the following journal.
Name: Nigerian journal of physiological sciences : official publication of the Physiological Society of Nigeria
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Maintenance of a constant blood glucose level by perfusion or infusion with glucose or insulin. It is used for the study of metabolic rates (e.g., in glucose, lipid, amino acid metabolism) at constant glucose concentration.
A metabolic process that converts GLUCOSE into two molecules of PYRUVIC ACID through a series of enzymatic reactions. Energy generated by this process is conserved in two molecules of ATP. Glycolysis is the universal catabolic pathway for glucose, free glucose, or glucose derived from complex CARBOHYDRATES, such as GLYCOGEN and STARCH.
The founding member of the sodium glucose transport proteins. It is predominately expressed in the INTESTINAL MUCOSA of the SMALL INTESTINE.
Volume of biological fluid completely cleared of drug metabolites as measured in unit time. Elimination occurs as a result of metabolic processes in the kidney, liver, saliva, sweat, intestine, heart, brain, or other site.
A glucose transport facilitator that is expressed primarily in PANCREATIC BETA CELLS; LIVER; and KIDNEYS. It may function as a GLUCOSE sensor to regulate INSULIN release and glucose HOMEOSTASIS.