Glycogen: its mode of formation and contribution to hepatic glucose output in postabsorptive humans

Pimenta, W P; Nurjhan, Nurjahan; Jansson, Per Anders; Stümvoll, Michael; Gerich, John E.; Korytkowski, Mary T.

doi:10.1007/bf00417694

Cited by 14 publications

(3 citation statements)

References 25 publications

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“…Previous estimates of indirect pathway glycogen formation in humans have ranged from 23 to 60% (34, 35, 46-48, 50, 54, 58). Our data are compatible with those of Pimenta et al (47), Peterson et al (46), and Magnusson et al (34,35), who found the indirect pathway to account for 33, 37, 23, and 35%, respectively, of overall glycogen formation.…”

Section: Discussionsupporting

confidence: 83%

Pathways for glucose disposal after meal ingestion in humans

Woerle¹,

Meyer²,

Dostou³

et al. 2003

American Journal of Physiology-Endocrinology and Metabolism

116

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To characterize postprandial glucose disposal more completely, we used the tritiated water technique, a triple-isotope approach (intravenous [3-H3]glucose and [14C]bicarbonate and oral [6,6-2H2]glucose) and indirect calorimetry to assess splanchnic and peripheral glucose disposal, direct and indirect glucose storage, oxidative and nonoxidative glycolysis, and the glucose entering plasma via gluconeogenesis after ingestion of a meal in 11 normal volunteers. During a 6-h postprandial period, a total of ∼98 g of glucose were disposed of. This was more than the glucose contained in the meal (∼78 g) due to persistent endogenous glucose release (∼21 g): splanchnic tissues initially took up ∼23 g, and an additional ∼75 g were removed from the systemic circulation. Direct glucose storage accounted for ∼32 g and glycolysis for ∼66 g (oxidative ∼43 g and nonoxidative ∼23 g). About 11 g of glucose appeared in plasma as a result of gluconeogenesis. If these carbons were wholly from glucose undergoing glycolysis, only ∼12 g would be available for indirect pathway glycogen formation. Our results thus indicate that glycolysis is the main initial postprandial fate of glucose, accounting for ∼66% of overall disposal; oxidation and storage each account for ∼45%. The majority of glycogen is formed via the direct pathway (∼73%).

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Section: Discussionsupporting

confidence: 83%

Pathways for glucose disposal after meal ingestion in humans

Woerle¹,

Meyer²,

Dostou³

et al. 2003

American Journal of Physiology-Endocrinology and Metabolism

116

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“…Determinations of the contribution of gluconeogenesis to glucose production in healthy subjects after an overnight fast have ranged from 25 to 70% (19,(33)(34)(35)(36)(37)(38)(39)(40)(41). That spread may be attributed in part to dietary preparation, but even with the same preparation, there has been marked variation in glycogen stores at the beginning of fasting (34).…”

Section: Discussionmentioning

confidence: 99%

Contributions of gluconeogenesis to glucose production in the fasted state.

et al. 1996

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Healthy subjects ingested 2 H 2 O and after 14, 22, and 42 h of fasting the enrichments of deuterium in the hydrogens bound to carbons 2, 5, and 6 of blood glucose and in body water were determined. The hydrogens bound to the carbons were isolated in formaldehyde which was converted to hexamethylenetetramine for assay. Enrichment of the deuterium bound to carbon 5 of glucose to that in water or to carbon 2 directly equals the fraction of glucose formed by gluconeogenesis. The contribution of gluconeogenesis to glucose production was 47 Ϯ 4% after 14 h, 67 Ϯ 4% after 22 h, and 93 Ϯ 2% after 42 h of fasting. Glycerol's conversion to glucose is included in estimates using the enrichment at carbon 5, but not carbon 6. Equilibrations with water of the hydrogens bound to carbon 3 of pyruvate that become those bound to carbon 6 of glucose and of the hydrogen at carbon 2 of glucose produced via glycogenolysis are estimated from the enrichments to be ‫ف‬ 80% complete. Thus, rates of gluconeogenesis can be determined without corrections required in other tracer methodologies. After an overnight fast gluconeogenesis accounts for ‫ف‬ 50% and after 42 h of fasting for almost all of glucose production in healthy subjects. ( J. Clin. Invest. 1996. 98:378-385.)

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“…More recently, Rothman et al (27), Petersen et al (28), and Magnusson et al (29) have quantified gluconeogenesis indirectly by subtracting the rate of hepatic glycogenolysis, measured by magnetic resonance imaging, from the tracer isotopemeasured rate of glucose production. Other methods have used glycogen-labeling technique (30) and mass isotopomer distribution analysis using [U-13 C]glucose tracer (31). All of these methods have resulted in estimates of gluconeogenesis in normal healthy subjects during the postabsorptive state to be in the range of 25 to 60%.…”

Section: Discussionmentioning

confidence: 99%

Glucose turnover and gluconeogenesis in human pregnancy.

Kalhan¹,

Rossi²,

Gruca³

et al. 1997

J. Clin. Invest.

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The rate of appearance (Ra) of glucose in plasma and the contribution of gluconeogenesis were quantified in normal pregnant women early ( ‫ف‬ 10 wk) and late ( ‫ف‬ 34 wk) in gestation. Their data were compared with those of normal nonpregnant women. Glucose Ra was measured using the [U Ϫ 13 C]glucose tracer dilution method. Gluconeogenesis was quantified by the appearance of 2 H on carbon 5 and 6 of glucose after deuterium labeling of body water pool. Weightspecific glucose Ra was unchanged during pregnancy (nonpregnant, 1.89 Ϯ 0.24; first trimester, 2.05 Ϯ 0.21; and third trimester 2.17 Ϯ 0.28 mg/kg·min, mean Ϯ SD), while total glucose Ra was significantly increased (early, 133.5 Ϯ 7.2; late, 162.6 Ϯ 16.4 mg/min; P ϭ 0.005). The fractional contribution of gluconeogenesis via pyruvate measured by 2 H enrichment on C-6 of glucose (45-61%), and of total gluconeogenesis quantified from 2 H enrichment on C-5 of glucose (i.e., including glycerol [68-85%]) was not significantly different between pregnant and nonpregnant women. Inasmuch as total glucose Ra was significantly increased, total gluconeogenesis was also increased in pregnancy (early pregnancy, 94.7 Ϯ 15.9 mg/min; late pregnancy, 122.7 Ϯ 9.3 mg/min; P ϭ 0.003). These data demonstrate the ability of the mother to adapt to the increasing fetal demands for glucose with advancing gestation. The mechanism for this unique quantitative adjustment to the fetal demands remains undefined. ( J. Clin. Invest. 1997. 100:1775-1781.)

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Glycogen: its mode of formation and contribution to hepatic glucose output in postabsorptive humans

Cited by 14 publications

References 25 publications

Pathways for glucose disposal after meal ingestion in humans

Pathways for glucose disposal after meal ingestion in humans

Contributions of gluconeogenesis to glucose production in the fasted state.

Glucose turnover and gluconeogenesis in human pregnancy.

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