Regulation of Cerebral Glucose Metabolism in Normal and Polycythemic Newborn Lambs

In contrast to previous investigations, a recent study of polycythemic lambs suggested that cerebral glucose delivery (concentration × blood flow), not arterial glucose concentration, determined cerebral glucose uptake. In the present study, the independent effects of arterial glucose concentration and delivery on cerebral glucose uptake were examined in two groups of chronically catheterized newborn lambs (control and polycythemic). Arterial glucose concentration was varied by an infusion of insulin. CBF was reduced in one group of lambs (polycythemic) by increasing the hematocrit. At all arterial glucose concentrations, the cerebral glucose delivery of the polycythemic group was 59.6% of the control group. At arterial glucose concentrations of > 1.6 mmol/L, cerebral glucose uptake was constant and similar in both groups. At arterial glucose concentrations of ≤1.6 mmol/L, cerebral glucose uptake was unchanged in the control group, but was significantly decreased in the polycythemic group. In contrast, the cerebral glucose uptake was similar in both groups over a broad range of cerebral glucose delivery values. At cerebral glucose delivery values ≤83 μmol/min/100 g, there was a significant decrease in cerebral glucose uptake in both groups. During periods of low cerebral glucose delivery and uptake, cerebral oxygen uptake fell in the control group but remained unchanged in the polycythemic group. Maintenance of cerebral oxygen uptake in the polycythemic group was associated with an increased extraction and uptake of lactate and β-hydroxybutyrate. We conclude that cerebral glucose delivery, not arterial glucose concentration alone, determines cerebral glucose uptake.

Download Full-text

Cerebral glucose metabolism and Cerebral blood flow in Hypothyroidism and Hyperthyroidism: An activation likelihood estimation Meta-analysis

Endocrine Abstracts ◽

10.1530/endoabs.63.p172 ◽

2019 ◽

Author(s):

Kyoungjune Pak ◽

Bo hyun Kim ◽

Mijin Kim ◽

Keunyoung Kim

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Glucose Metabolism ◽

Meta Analysis ◽

Likelihood Estimation ◽

Cerebral Glucose Metabolism ◽

Activation Likelihood Estimation

Download Full-text

Influence of endogenous norepinephrine on cerebral blood flow and metabolism

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1976.231.2.489 ◽

1976 ◽

Vol 231 (2) ◽

pp. 489-494 ◽

Cited By ~ 112

Author(s):

ET MacKenzie ◽

J McCulloch ◽

AM Harper

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Oxygen Consumption ◽

Glucose Uptake ◽

Cerebral Circulation ◽

Brain Metabolism ◽

Cerebral Metabolism ◽

Cerebral Oxygen ◽

Brain Norepinephrine ◽

Cerebral Oxygen Consumption

The influence of brain norepinephrine on cerebral metabolism and blood flow was examined because exogenous norepinephrine, administered in a way that the blood-brain barrier is bypassed, has been shown to effect pronounced changes in the cerebral circulation. Reserpine (40 mug/kg, by intracarotid infusion) was administered in order to release brain norepinephrine in five anesthetized baboons. Reserpine significantly increased cerebral oxygen consumption (23%) and cerebral blood flow (50%). This response lasted for approximately 60 min. In a further five animals, effects of central beta-adrenoreceptor blockade were studied. Pro pranolol (12 mug/kg-min) produced an immediate, significant reduction in both cerebral oxygen consumption (40%) and cerebral glucose uptake (39%). Cerebral blood flow was reduced minimally. However, the responsiveness of the cerebral circulation to induced hypercapnia was severely attenuated from a gradient of 3.22 before, to 1,11 after, administration. These experiments suggest that central norepinephrine can influence the cerebral circulation primarily through noradrenergic effects on brain metabolism.

Download Full-text

In vitro analysis of glucose metabolism and embryonic growth in postimplantation rat embryos

Development ◽

10.1242/dev.100.3.431 ◽

1987 ◽

Vol 100 (3) ◽

pp. 431-439 ◽

Cited By ~ 1

Author(s):

S.K. Ellington

Keyword(s):

Glucose Metabolism ◽

Embryonic Development ◽

Glucose Uptake ◽

Glucose Concentration ◽

Culture Media ◽

Rat Embryos ◽

Embryonic Growth ◽

Stage Of Development

The glucose metabolism and embryonic development of rat embryos during organogenesis was studied using embryo culture. Glucose uptake and embryonic growth and differentiation of 10.5-day explants (embryos + membranes) were limited by the decreasing glucose concentration, but not the increasing concentration of metabolites, in the culture media during the second 24 h of a 48 h culture. No such limitations were found on the embryonic development of 9.5-day explants during a 48 h culture although glucose uptake was slightly reduced at very low concentrations of glucose. From the head-fold stage to the 25-somite stage of development, glucose uptake was characteristic of the stage of development of the embryo and not the time it had been in culture. Embryonic growth of 9.5-day explants was similar to that previously observed in vivo. Glucose uptake by 9.5-day explants was dependent on the surface area of the yolk sac and was independent of the glucose concentration in the culture media (within the range of 9.4 to 2.5 mM). The proportion of glucose converted to lactate was 100% during the first 42h of culture then fell to about 50% during the final 6h. The protein contents of both the extraembryonic membranes and the embryo were dependent on the glucose uptake.

Download Full-text

Author Correction: Cerebral glucose metabolism and Cerebral blood flow in thyroid dysfunction: An Activation Likelihood Estimation Meta-analysis

Scientific Reports ◽

10.1038/s41598-020-62219-0 ◽

2020 ◽

Vol 10 (1) ◽

Author(s):

Kyoungjune Pak ◽

Mijin Kim ◽

Keunyoung Kim ◽

Bo Hyun Kim ◽

Seong-Jang Kim ◽

...

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Glucose Metabolism ◽

Thyroid Dysfunction ◽

Meta Analysis ◽

Likelihood Estimation ◽

Cerebral Glucose Metabolism ◽

Activation Likelihood Estimation

Download Full-text

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

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.2000.279.2.e284 ◽

2000 ◽

Vol 279 (2) ◽

pp. E284-E292 ◽

Cited By ~ 8

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.

Download Full-text

Intraportal administration of neuropeptide Y and hepatic glucose metabolism

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00903.2007 ◽

2008 ◽

Vol 294 (4) ◽

pp. R1197-R1204 ◽

Cited By ~ 3

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.

Download Full-text