Effects of Arterial-Portal Glucose Difference on Gluconeogenesis from Lactate in the Isolated Bivascular-Perfused Rat Liver

Mokuda, O; Sakamoto, Yoshikazu; Kawagoe, Rika; Shimizu, Norihiro

doi:10.1055/s-2007-1002099

Cited by 6 publications

(4 citation statements)

References 12 publications

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“…Incorporation of 14 C lactate into glucose in perfusion was assayed according to a previously reported method [9]. Briefly, perfusate was deproteinized and boiled to liberate CO 2 gas.…”

Section: Gluconeogenesismentioning

confidence: 99%

Ethanol Stimulates Glycogenolysis and Inhibits both Glycogenesis via Gluconeogenesis and from Exogenous Glucose in Perfused Rat Liver

Mokuda¹,

Tanaka²,

Hayashi³

et al. 2004

Ann Nutr Metab

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Aims: Although it is commonly recognized that ethanol suppresses gluconeogenesis, the influence of alcohol intake on blood glucose levels remains controversial. Ethanol may act on both glucose production and glucose consumption in the liver. Thus, we studied each effect of ethanol on glucose oxidation, gluconeogenesis, glycogenesis and glycogenolysis in the liver. Methods: The rat liver was isolated and cyclically perfused with a medium containing 50 mmol/l ethanol. Results: Ethanol enhanced ¹⁴C-glucose oxidation in the liver from 1.09 ± 0.11 to 1.41 ± 0.14 µmol for 20 min (p < 0.05). Gluconeogenesis from ¹⁴C-lactate was markedly reduced by ethanol from 8.0 ± 1.3 to 1.5 ± 0.6 µmol for 12 min (p < 0.01). Ethanol increased glycogenolysis (net hepatic glucose output, 0.47 ± 0.10 vs. 0.22 ± 0.04 mmol/30 min, p < 0.01), and then decreased hepatic glycogen content (179 ± 38 vs. 273 ± 39 mg in the presence of 1 mU/ml insulin after 30 min of perfusion, p < 0.05). Ethanol decreased the direct glycogenesis from ¹⁴C-glucose from 0.55 ± 0.08 to 0.33 ± 0.05 µmol per 100 mg glycogen for 30 min (p < 0.01). Ethanol inhibited the indirect glycogenesis from ¹⁴C-lactate from 0.21 ± 0.04 to 0.09 ± 0.01 µmol per 100 mg glycogen for 30 min (p < 0.01). Discussion: The influence of ethanol on the blood glucose regulation by the liver seems to be different between fasted and fed states. Namely, ethanol has both the hypoglycemic effects through decreased gluconeogenesis and increased glucose oxidation and the hyperglycemic effects through decreased glycogenesis and increased glycogenolysis.

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“…Incorporation of 14 C lactate into glucose in perfusion was assayed according to a previously reported method [9]. Briefly, perfusate was deproteinized and boiled to liberate CO 2 gas.…”

Section: Gluconeogenesismentioning

confidence: 99%

Ethanol Stimulates Glycogenolysis and Inhibits both Glycogenesis via Gluconeogenesis and from Exogenous Glucose in Perfused Rat Liver

Mokuda¹,

Tanaka²,

Hayashi³

et al. 2004

Ann Nutr Metab

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“…The disposal of this excess glucose falls largely on the white adipose tissue (WAT), which is already strained by the excess lipid [7], thereby favoring glycolysis and lactate production [21]. The excess lactate is used by the liver for gluconeogenesis [22] or lipid synthesis [23] (Fig. 1).…”

Section: The Pathognomic Links: Insulin Resistancementioning

confidence: 99%

Metabolic Syndrome: A Multifaceted Disease of Affluence

Alemany

2012

J Endocrinol Metab

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Metabolic syndrome developed in consequence of an evolutionary inadequacy: the human body was unprepared for a dietary excess of nutrients, especially lipids (largely in detriment of carbohydrate). This excess awakens metabolic signals akin to those of starvation, in which the main energy staple is the body's own lipid reserve. Lipid dietary abundance prevents the use of glucose, which in turn limits the oxidation of amino acids. To ward against a subsequent avalanche of substrates, the immune system and hypertrophied tissues (for example, adipose) elicit a series of defence responses. This response is probably the ultimate basis of a disease that is manifested as various pathologies, which were initially defined as distinct entities but which are slowly being seen as a single pathognomic unit in the literature. Based on their common origin of the ample availability of food in our modern society, the cluster of diseases comprising the metabolic syndrome is probably best described as a single multifaceted disease.

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“…Pancreas and liver were perfused according to the previously reported methods (Mokuda and Sakamoto, 1998;Mokuda et al, 1993). The pancreas was perfused at a rate of 4 ml/min.…”

Section: Pancreas and Liver Perfusionmentioning

confidence: 99%

“…Insulin values were determined by the use of a rat insulin standard (Cosmo Bio, Tokyo) and the other components of a radioimmunoassay kit (Shionogi, Osaka) with its intra-and interassay CV of 5.8% and 5.2%. Perfusate glucose-1-14 C was measured by the previously reported method (Mokuda et al, 1993). Briefly, perfusate was deproteinized and boiled to liberate CO 2 gas.…”

Section: Analysesmentioning

confidence: 99%

Acidotic pH augments glucagon secretion and gluconeogenesis in the isolated perfused rat pancreas and liver

Mokuda¹,

Sakamoto²

2000

Exp Clin Endocrinol Diabetes

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To study effects of acidosis on glucagon secretion and gluconeogenetic action of glucagon, rat pancreas and liver were perfused with media of pH 6.4, 6.9, 7.4 and 7.9. Glucagon secretion from the pancreas during glucopenic perfusion (1 mmol/l) was blunted at alkalotic pH, and was augmented at acidotic pH; 0.28+/-0.18 at pH 7.9 (P<0.01), 3.57+/-0.94 at pH 6.9 (P<0.01) and 1.72+/-0.36 at pH 6.4 (P<0.01), vs. 0.66+/-0.25 pmol for 15 min at pH 7.4. Incorporation rate of 14C of lactate-U-14C into glucose carbon one was decreased at pH 7.9 (1.2+/-0.2% for 15 min, P<0.05) and was increased at pH 6.9 (2.8+/-0.5%, P<0.05) compared to that at pH 7.4 (1.9+/-0.3%). Percent increasing rate of lactate gluconeogenesis by 1 nmol/l glucagon was not different within a range of pH 6.4-7.9. Thus, glucagon-stimulated gluconeogenesis from lactate was smaller at pH 7.9 (2.2+/-0.6%) and was significantly greater at pH 6.9 (4.9+/-0.9%, P<0.05) than that at pH 7.4 (3.2+/-0.6%). These results suggest that the pancreatic glucagon secretion and the glucagon-stimulated hepatic gluconeogenesis play more important roles in the maintainance of blood glucose level in the stress states associated with acidosis than without acidosis.

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Effects of Arterial-Portal Glucose Difference on Gluconeogenesis from Lactate in the Isolated Bivascular-Perfused Rat Liver

Cited by 6 publications

References 12 publications

Ethanol Stimulates Glycogenolysis and Inhibits both Glycogenesis via Gluconeogenesis and from Exogenous Glucose in Perfused Rat Liver

Ethanol Stimulates Glycogenolysis and Inhibits both Glycogenesis via Gluconeogenesis and from Exogenous Glucose in Perfused Rat Liver

Metabolic Syndrome: A Multifaceted Disease of Affluence

Acidotic pH augments glucagon secretion and gluconeogenesis in the isolated perfused rat pancreas and liver

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