Rapid altering light cycles promotes increased hepatic glucose uptake and de novo lipogenesis

2019 ◽  
Vol 13 (1) ◽  
pp. 75-76
Author(s):  
Stewart D. Christie ◽  
Rebecca J. O-Rielly ◽  
Claudine L. Frisby ◽  
Nichola Thompson ◽  
Amanda J. Page ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
De Novo ◽  
De Novo Lipogenesis ◽  
Hepatic Glucose ◽  
Hepatic Glucose Uptake

scholarly journals Quantitative Determination of Hepatic Glucose Uptake Using an Innovative Approach

1991 ◽  
Vol 37 (Supplement) ◽  
pp. S35-S42 ◽  
Author(s):  
Ryuzo KAWAMORI ◽  
Minoru KUBOTA ◽  
Masahiko IKEDA ◽  
Munehide MATSUHISA ◽  
Masashi KUBOTA ◽  
...  
Keyword(s):  
Quantitative Determination ◽  
Glucose Uptake ◽  
Innovative Approach ◽  
Hepatic Glucose ◽  
Hepatic Glucose Uptake

scholarly journals Nonhepatic response to portal glucose delivery in conscious dogs

2000 ◽  
Vol 279 (6) ◽  
pp. E1271-E1277 ◽  
Author(s):  
Mary Courtney Moore ◽  
Po-Shiuan Hsieh ◽  
Doss W. Neal ◽  
Alan D. Cherrington
Keyword(s):  
Glucose Uptake ◽  
Glucose Infusion ◽  
Glucose Load ◽  
Arterial Blood ◽  
Hepatic Glucose ◽  
The Difference ◽  
Arterial Plasma ◽  
Arterial Blood Glucose ◽  
Blood Glucose Concentrations ◽  
Hepatic Glucose Uptake

The glycemic and hormonal responses and net hepatic and nonhepatic glucose uptakes were quantified in conscious 42-h-fasted dogs during a 180-min infusion of glucose at 10 mg · kg−1 · min−1 via a peripheral (Pe10, n = 5) or the portal (Po10, n = 6) vein. Arterial plasma insulin concentrations were not different during the glucose infusion in Pe10 and Po10 (37 ± 6 and 43 ± 12 μU/ml, respectively), and glucagon concentrations declined similarly throughout the two studies. Arterial blood glucose concentrations during glucose infusion were not different between groups (125 ± 13 and 120 ± 6 mg/dl in Pe10 and Po10, respectively). Portal glucose delivery made the hepatic glucose load significantly greater (36 ± 3 vs. 46 ± 5 mg · kg−1 · min−1 in Pe10 vs. Po10, respectively, P < 0.05). Net hepatic glucose uptake (NHGU; 1.1 ± 0.4 vs. 3.1 ± 0.4 mg · kg−1 · min−1) and fractional extraction (0.03 ± 0.01 vs. 0.07 ± 0.01) were smaller ( P < 0.05) in Pe10 than in Po10. Nonhepatic (primarily muscle) glucose uptake was correspondingly increased in Pe10 compared with Po10 (8.9 ± 0.4 vs. 6.9 ± 0.4 mg · kg−1 · min−1, P < 0.05). Approximately one-half of the difference in NHGU between groups could be accounted for by the difference in hepatic glucose load, with the remainder attributable to the effect of the portal signal itself. Even in the absence of somatostatin and fixed hormone concentrations, the portal signal acts to alter partitioning of a glucose load among the tissues, stimulating NHGU and reducing peripheral glucose uptake.

Intrahepatic glucose: a requirement for neonatal ODC induction by specific hormones

1984 ◽  
Vol 247 (2) ◽  
pp. E243-E250
Author(s):  
G. Evoniuk ◽  
C. Kuhn ◽  
S. Schanberg
Keyword(s):  
Glucose Uptake ◽  
Intragastric Administration ◽  
Nutritional Deprivation ◽  
Rat Pups ◽  
Absolute Requirement ◽  
Whole Milk ◽  
Hepatic Glucose ◽  
Nutrient Administration ◽  
Hepatic Glucose Uptake

We have shown previously that short-term nutritional deprivation causes a tissue-specific loss of liver ornithine decarboxylase (ODC) induction after isoproterenol, phenylephrine, or glucagon administration in rat pups. To examine the role of nutrition in the regulation of hepatic ODC, we tested the ability of intragastric nutrient administration to reverse nutritionally related deficits in the ODC response to hormonal challenge. Intragastric whole milk was effective in restoring ODC induction and accumulation of its immediate product, putrescine, in response to isoproterenol administration. Glucose was shown to mediate this effect by the ability of intragastric skimmed milk, lactose, galactose, or D-glucose to return ODC induction, and the inability of casein, sucrose, fructose, L-glucose, or pyruvate plus lactate to do so. D-Glucose also reestablished ODC induction by phenylephrine and glucagon. Parenteral administration of D-glucose produced results comparable to those obtained after intragastric administration. Isoproterenol induction of ODC was prevented when hepatic glucose uptake was blocked by phlorizin but not by blockade of central nervous system glucose uptake with 2-deoxyglucose. We conclude that intrahepatic glucose is an absolute requirement for hepatic ODC induction by isoproterenol, phenylephrine, or glucagon in preweanling rats.

Rapid reversal of the effects of the portal signal under hyperinsulinemic conditions in the conscious dog

1999 ◽  
Vol 276 (5) ◽  
pp. E930-E937 ◽  
Author(s):  
Po-Shiuan Hsieh ◽  
Mary Courtney Moore ◽  
Doss W. Neal ◽  
Maya Emshwiller ◽  
Alan D. Cherrington
Keyword(s):  
Glucose Uptake ◽  
Infusion Rate ◽  
Experimental Period ◽  
Glucose Infusion ◽  
Glucose Load ◽  
Conscious Dog ◽  
The Third ◽  
Hepatic Glucose ◽  
Rapid Reversal ◽  
Hepatic Glucose Uptake

Experiments were performed on two groups of 42-h-fasted conscious dogs ( n = 6/group). Somatostatin was given peripherally with insulin (4-fold basal) and glucagon (basal) intraportally. In the first experimental period, glucose was infused peripherally to double the hepatic glucose load (HGL) in both groups. In the second experimental period, glucose (21.8 μmol ⋅ kg−1⋅ min−1) was infused intraportally and the peripheral glucose infusion rate (PeGIR) was reduced to maintain the precreating HGL in the portal signal (PO) group, whereas saline was given intraportally in the control (CON) group and PeGIR was not changed. In the third period, the portal glucose infusion was stopped in the PO group and PeGIR was increased to sustain HGL. PeGIR was continued in the CON group. The glucose loads to the liver did not differ in the CON and PO groups. Net hepatic glucose uptake was 9.6 ± 2.5, 11.6 ± 2.6, and 15.5 ± 3.2 vs. 10.8 ± 1.8, 23.7 ± 3.0, and 15.5 ± 1.1 μmol ⋅ kg−1⋅ min−1, and nonhepatic glucose uptake (non-HGU) was 29.8 ± 1.1, 40.1 ± 4.5, and 49.5 ± 4.0 vs. 26.6 ± 4.3, 23.2 ± 4.0, and 40.4 ± 3.1 μmol ⋅ kg−1⋅ min−1in the CON and PO groups during the three periods, respectively. Cessation of the portal signal shifted NHGU and non-HGU to rates similar to those evident in the CON group within 10 min. These results indicate that even under hyperinsulinemic conditions the effects of the portal signal on hepatic and peripheral glucose uptake are rapidly reversible.

Importance of the hepatic arterial glucose level in generation of the portal signal in conscious dogs

2000 ◽  
Vol 279 (2) ◽  
pp. E284-E292 ◽  
Author(s):  
Po-Shiuan Hsieh ◽  
Mary Courtney Moore ◽  
Doss W. Neal ◽  
Alan D. Cherrington
Keyword(s):  
Glucose Uptake ◽  
Hepatic Artery ◽  
Glucose Level ◽  
Test Period ◽  
Conscious Dogs ◽  
Control Group ◽  
Period 2 ◽  
Hepatic Glucose ◽  
Hepatic Glucose Uptake ◽  
Arterial Glucose

The aim of this study was to determine whether the elimination of the hepatic arterial-portal (A-P) venous glucose gradient would alter the effects of portal glucose delivery on hepatic or peripheral glucose uptake. Three groups of 42-h-fasted conscious dogs ( n = 7/group) were studied. After a 40-min basal period, somatostatin was infused peripherally along with intraportal insulin (7.2 pmol·kg−1·min−1) and glucagon (0.65 ng·kg−1·min−1). In test period 1 (90 min), glucose was infused into a peripheral vein to double the hepatic glucose load (HGL) in all groups. In test period 2 (90 min) of the control group (CONT), saline was infused intraportally; in the other two groups, glucose was infused intraportally (22.2 μmol·kg−1·min−1). In the second group (PD), saline was simultaneously infused into the hepatic artery; in the third group (PD+HAD), glucose was infused into the hepatic artery to eliminate the negative hepatic A-P glucose gradient. HGL was twofold basal in each test period. Net hepatic glucose uptake (NHGU) was 10.1 ± 2.2 and 12.8 ± 2.1 vs. 11.5 ± 1.6 and 23.8 ± 3.3* vs. 9.0 ± 2.4 and 13.8 ± 4.2 μmol · kg−1·min−1 in the two periods of CONT, PD, and PD+HAD, respectively (*  P < 0.05 vs. same test period in PD and PD+HAD). NHGU was 28.9 ± 1.2 and 39.5 ± 4.3 vs. 26.3 ± 3.7 and 24.5 ± 3.7* vs. 36.1 ± 3.8 and 53.3 ± 8.5 μmol·kg−1·min−1 in the first and second periods of CONT, PD, and PD+HAD, respectively (*  P < 0.05 vs. same test period in PD and PD+HAD). Thus the increment in NHGU and decrement in extrahepatic glucose uptake caused by the portal signal were significantly reduced by hepatic arterial glucose infusion. These results suggest that the hepatic arterial glucose level plays an important role in generation of the effect of portal glucose delivery on glucose uptake by liver and muscle.

Infection impairs insulin-dependent hepatic glucose uptake during total parenteral nutrition

2003 ◽  
Vol 284 (3) ◽  
pp. E574-E582 ◽  
Author(s):  
Christine M. Donmoyer ◽  
Sheng-Song Chen ◽  
D. Brooks Lacy ◽  
David A. Pearson ◽  
Adrian Poole ◽  
...  
Keyword(s):  
Parenteral Nutrition ◽  
Glucose Uptake ◽  
Total Parenteral Nutrition ◽  
Insulin Treatment ◽  
Second Step ◽  
Sham Surgery ◽  
Hepatic Glucose ◽  
Mild Hyperglycemia ◽  
Insulin Dependent ◽  
Hepatic Glucose Uptake

Total parenteral nutrition (TPN) markedly augments net hepatic glucose uptake (NHGU) and hepatic glycolysis in the presence of mild hyperglycemia and hyperinsulinemia. This increase is impaired by an infection. We determined whether the adaptation to TPN alters the responsiveness of the liver to insulin and whether infection impairs that response. Chronically catheterized dogs received TPN for 5 days. On day 3 of TPN, either a nonlethal hypermetabolic infection was induced (INF, n = 5) or a sham surgery was performed (SHAM, n = 5). Forty-two hours after clot implantation, somatostatin and glucagon (34 ± 3 vs. 84 ± 11 pg/ml in artery, SHAM vs. INF) were infused, and a three-step (120 min each) isoglycemic (∼120 mg/dl) hyperinsulinemic (∼12, 25, and 50 μU/ml) clamp was performed to simulate levels seen in normal, infected, and exogenous insulin treatment states. In SHAM, NHGU (3.5 ± 0.2 to 4.2 ± 0.4 to 4.6 ± 0.5 mg · kg−1· min−1) modestly increased. In INF, NHGU was consistently lower at each insulin step (1.1 ± 0.5 to 2.6 ± 0.5 to 2.8 ± 0.7 mg · kg−1· min−1). Although NHGU increased from the first to the second step in INF, it did not increase further with the highest dose of insulin. Despite increases in NHGU, net hepatic lactate release did not increase in SHAM and fell in INF. In summary, in the TPN-adapted state, liver glucose uptake is unresponsive to increases in insulin above the basal level. Although the infection-induced increase in insulin sustains NHGU, further increments in insulin enhance neither NHGU nor glycolysis.

Intraportal administration of neuropeptide Y and hepatic glucose metabolism

2008 ◽  
Vol 294 (4) ◽  
pp. R1197-R1204 ◽  
Author(s):  
Makoto Nishizawa ◽  
Masakazu Shiota ◽  
Mary Courtney Moore ◽  
Stephanie M. Gustavson ◽  
Doss W. Neal ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Neuropeptide Y ◽  
Glucose Uptake ◽  
Infusion Rate ◽  
Whole Body ◽  
Glucose Disposal ◽  
Control Group ◽  
Intravenous Glucose ◽  
Hepatic Glucose ◽  
Hepatic Glucose Uptake

We examined whether intraportal delivery of neuropeptide Y (NPY) affects glucose metabolism in 42-h-fasted conscious dogs using arteriovenous difference methodology. The experimental period was divided into three subperiods (P1, P2, and P3). During all subperiods, the dogs received infusions of somatostatin, intraportal insulin (threefold basal), intraportal glucagon (basal), and peripheral intravenous glucose to increase the hepatic glucose load twofold basal. Following P1, in the NPY group ( n = 7), NPY was infused intraportally at 0.2 and 5.1 pmol·kg−1·min−1 during P2 and P3, respectively. The control group ( n = 7) received intraportal saline infusion without NPY. There were no significant changes in hepatic blood flow in NPY vs. control. The lower infusion rate of NPY (P2) did not enhance net hepatic glucose uptake. During P3, the increment in net hepatic glucose uptake (compared with P1) was 4 ± 1 and 10 ± 2 μmol·kg−1·min−1 in control and NPY, respectively ( P < 0.05). The increment in net hepatic fractional glucose extraction during P3 was 0.015 ± 0.005 and 0.039 ± 0.008 in control and NPY, respectively ( P < 0.05). Net hepatic carbon retention was enhanced in NPY vs. control (22 ± 2 vs. 14 ± 2 μmol·kg−1·min−1, P < 0.05). There were no significant differences between groups in the total glucose infusion rate. Thus, intraportal NPY stimulates net hepatic glucose uptake without significantly altering whole body glucose disposal in dogs.

Hepatic glucose metabolism during intraduodenal glucose infusion: impact of infection

2000 ◽  
Vol 279 (1) ◽  
pp. E108-E115
Author(s):  
Owen P. McGuinness ◽  
Joseph Ejiofor ◽  
D. Brooks Lacy ◽  
Nancy Schrom
Keyword(s):  
Glucose Metabolism ◽  
Glucose Uptake ◽  
Glycogen Synthesis ◽  
Fibrin Clot ◽  
Glucose Absorption ◽  
Glucose Infusion ◽  
Hepatic Glucose Metabolism ◽  
Hepatic Glucose ◽  
Glycogen Deposition ◽  
Hepatic Glucose Uptake

We previously reported that infection decreases hepatic glucose uptake when glucose is given as a constant peripheral glucose infusion (8 mg · kg−1· min−1). This impairment persisted despite greater hyperinsulinemia in the infected group. In a normal setting, hepatic glucose uptake can be further enhanced if glucose is given gastrointestinally. Thus the aim of this study was to determine whether hepatic glucose uptake is impaired during an infection when glucose is given gastrointestinally. Thirty-six hours before study, a sham (SH, n = 7) or Escherichia coli-containing (2 × 109organisms/kg; INF; n = 7) fibrin clot was placed in the peritoneal cavity of chronically catheterized dogs. After the 36 h, a glucose bolus (150 mg/kg) followed by a continuous infusion (8 mg · kg−1· min−1) of glucose was given intraduodenally to conscious dogs for 240 min. Tracer ([3-3H]glucose and [U-14C]glucose) and arterial-venous difference techniques were used to assess hepatic and intestinal glucose metabolism. Infection increased hepatic blood flow (35 ± 5 vs. 47 ± 3 ml · kg−1· min−1; SH vs. INF) and basal glucose rate of appearance (2.1 ± 0.2 vs. 3.3 ± 0.1 mg · kg−1· min−1). Arterial insulin concentrations increased similarly in SH and INF during the last hour of glucose infusion (38 ± 8 vs. 46 ± 20 μU/ml), and arterial glucagon concentrations fell (62 ± 14 to 30 ± 3 vs. 624 ± 191 to 208 ± 97 pg/ml). Net intestinal glucose absorption was decreased in INF, attenuating the increase in blood glucose caused by the glucose load. Despite this, net hepatic glucose uptake (1.6 ± 0.8 vs. 2.4 ± 0.9 mg · kg−1· min−1; SH vs. INF) and consequently tracer-determined glycogen synthesis (1.3 ± 0.3 vs. 1.0 ± 0.3 mg · kg−1· min−1) were similar between groups. In summary, infection impairs net glucose absorption, but not net hepatic glucose uptake or glycogen deposition, when glucose is given intraduodenally.

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