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Results: 1211 to 1220 of 1222

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Ketone body turnover and net hepatic ketone production in fasted and diabetic dogs.
Keller U, Cherrington AD, Liljenquist JE
(1978) Am J Physiol 235: E238-47
MeSH Terms: Acetoacetates, Alloxan, Animals, Blood Glucose, Diabetes Mellitus, Experimental, Dogs, Fasting, Fatty Acids, Nonesterified, Female, Glucagon, Hydroxybutyrates, Ketone Bodies, Liver, Male, Regional Blood Flow
Added December 10, 2013
0 Communities
1 Members
0 Resources
15 MeSH Terms
Glucose disposal during insulinopenia in somatostatin-treated dogs. The roles of glucose and glucagon.
Shulman GI, Liljenquist JE, Williams PE, Lacy WW, Cherrington AD
(1978) J Clin Invest 62: 487-91
MeSH Terms: Animals, Blood Glucose, Dogs, Female, Glucagon, Glucose, Insulin, Liver, Liver Glycogen, Male, Somatostatin
Show Abstract · Added February 13, 2015
The first aim of this study was to determine whether the plasma glucose level can regulate hepatic glucose balance in vivo independent of its effects on insulin and glucagon secretion. To accomplish this, glucose was infused into conscious dogs whose basal insulin and glucagon secretion had been replaced by exogenous intraportal insulin and glucagon infusion after somatostatin inhibition of endogenous pancreatic hormone release. The acute induction of hyperglycemia (mean increment of 121 mg/dl) in the presence of basal levels of insulin (7+/-1 muU/ml) and glucagon (76+/-3 pg/ml) resulted in a 56% decrease in net hepatic glucose production but did not cause net hepatic glucose uptake. The second aim of the study was to determine whether a decrease in the plasma glucagon level would modify the effect of glucose on the liver. The above protocol was repeated with the exception that glucagon was withdrawn (83% decrease in plasma glucagon) coincident with the induction of hyperglycemia. Under this circumstance, with the insulin level basal (7+/-1 muU/ml) and the glucagon levels reduced (16+/-2 pg/ml), hyperglycemia (mean increment of 130 mg/dl) promoted marked net hepatic glucose uptake (1.5+/-0.2 mg/kg per min) and glycogen deposition. In conclusion, (a) physiological increments in the plasma glucose concentration, independent of their effects on insulin and glucagon secretion, can significantly reduce net hepatic glucose production in vivo but at levels as high as 230 mg/dl cannot induce net hepatic glucose storage and (b) in the presence of basal insulin the ability of hyperglycemia to stimulate net hepatic glucose storage is influenced by the plasma glucagon concentration.
0 Communities
1 Members
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11 MeSH Terms
Relationship between the plasma glucose level and glucose uptake in the conscious dog.
Cherrington AD, Williams PE, Harris MS
(1978) Metabolism 27: 787-91
MeSH Terms: Animals, Blood Glucose, Dogs, Female, Glucose, Male, Metabolic Clearance Rate, Statistics as Topic
Show Abstract · Added December 10, 2013
In the absence of a change in the pancreatic hormonal milieu, elevations in the normal fasting plasma glucose level have little effect on glucose clearance. In view of these data, and the previously established responsiveness of M to hormones, glucose clearance can be considered to represent a useful index of hormone action on glucose uptake in vivo. Care should be taken, however, when interpreting clearance data obtained under hypoglycemic conditions, since there is a possibility that clearance may spontaneously increase at very low plasma glucose levels.
0 Communities
1 Members
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8 MeSH Terms
Possible mechanism by which somatostatin-induced glucagon suppression improves glucose tolerance during insulinopaenia in man.
Liljenquist JE, Bloomgarden ZT, Cherrington AD, Perry JM, Rabin D
(1979) Diabetologia 17: 139-43
MeSH Terms: Adolescent, Adult, Glucagon, Glucose, Glucose Tolerance Test, Humans, Hyperglycemia, Insulin, Male, Somatostatin
Added December 10, 2013
0 Communities
1 Members
0 Resources
10 MeSH Terms
Importance of hypoglycemia-induced glucose production during isolated glucagon deficiency.
Cherrington AD, Liljenquist JE, Shulman GI, Williams PE, Lacy WW
(1979) Am J Physiol 236: E263-71
MeSH Terms: Animals, Blood Glucose, Dogs, Female, Glucagon, Glucose, Male, Somatostatin, Time Factors
Added December 10, 2013
0 Communities
1 Members
0 Resources
9 MeSH Terms
Hyperglycemia per se (insulin and glucagon withdrawn) can inhibit hepatic glucose production in man.
Liljenquist JE, Mueller GL, Cherrington AD, Perry JM, Rabinowitz D
(1979) J Clin Endocrinol Metab 48: 171-5
MeSH Terms: Blood Glucose, Glucagon, Glucose, Humans, Hyperglycemia, Insulin, Liver, Male, Somatostatin
Show Abstract · Added December 10, 2013
We examined the effect of hyperglycemia per se on net splanchnic glucose balance. In 2 groups of normal postabsorptive men who had undergone hepatic vein catheterization, somatostatin was administered to block endogenous insulin and glucagon secretion. Exogenous glucose was infused in both groups to maintain euglycemia for 2 h in one group (n = 7) and to induce hyperglycemia of 220-240 mg/dl after 30 minutes of euglycemia in the second group (n = 4). In both groups the induction of insulinopenia and glucagonopenia with euglycemia maintained resulted in an initial 75% fall in net splanchnic glucose production (NSGP). In the group in which euglycemia was maintained NSGP returned to basal rates (157 +/- 31 mg/min) within 2 h. However, in the group in which hyperglycemia was induced, NSGP did not return to basal rates but remained suppressed (28 +/- 4 mg/min) for the duration of the study. These data in normal man indicate that hyperglycemia per se with insulin and glucagon acutely withdrawn can suppress splanchnic glucose production but does not induce net splanchnic glucose storage.
0 Communities
1 Members
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9 MeSH Terms
Control of hepatic glucose output by glucagon and insulin in the intact dog.
Cherrington AD, Chiasson JL, Liljenquist JE, Lacy WW, Park CR
(1978) Biochem Soc Symp : 31-45
MeSH Terms: Animals, Blood Glucose, Dogs, Glucagon, Gluconeogenesis, Glucose, Insulin, Liver, Liver Glycogen, Somatostatin, Time Factors
Show Abstract · Added December 10, 2013
The regulation of hepatic glucose production by glucagon and insulin has been studied in the intact dog. An attempt has been made to evaluate the role of basal physiological concentrations of the hormones in the regulation of glycogenolysis and gluconeogenesis. Somatostatin was infused continuously into postabsorptive dogs to inhibit the secretion of both glucagon and insulin. Either or both hormones were then replaced intraportally by continuous infusion as desired. The main observations were as follows. (1) When both hormones were simultaneously replaced for periods up to 4.5h, plasma insulin and glucagon concentrations, total glucose output (glycogenolysis plus gluconeogenesis), glucose utilization and the plasma glucose concentration closely matched the same parameters in 0.9% NaCl-infused controls. (2) When glucagon alone was infused, thereby creating a selective insulin deficiency, glucose output (primarily glycogenolysis) rapidly increased by as much as threefold. Glycogenolytic glucose production then fell off progressively and returned to the control value within 4h. The gluconeogenic conversion of [14C]alanine and [14C]lactate into [14C]glucose was stimulated markedly and increased progressively throughout the test period. Glucagon therefore converted the liver from an organ largely dependent on glycogenolysis for glucose production to one heavily dependent on gluconeogenesis. The potent inhibitory effect of basal insulin on postabsorptive glucose output was also clearly apparent. (3) When insulin alone was infused, thereby creating a selective glucagon deficiency, glucose output (glycogenolysis) fell abruptly by about 30% and remained decreased. Gluconeogenesis also decreased (20%) after the selective removal of both insulin and glucagon, but it only remained suppressed for 1h. The low glucose output led to a modest fall in the blood glucose concentration. Thus glucagon plays an important role in maintaining basal glucose production. (4) When insulin was infused and the plasma glucose was kept at its control concentration by infusion of glucose in similar experiments to the above, the hepatic output of glucose fell by as much as 75%. This demonstrates the presence of a glucagon-independent metabolic reflex triggered by a low plasma glucose concentration, the purpose of which is to maintain glucose output at a rate capable of preventing castastrophic hypoglycaemia.
0 Communities
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11 MeSH Terms
Gluconeogenesis: methodological approaches in vivo.
Chiasson JL, Liljenquist JE, Lacy WW, Jennings AS, Cherrington AD
(1977) Fed Proc 36: 229-35
MeSH Terms: Alanine, Animals, Autoradiography, Blood Glucose, Carbon Radioisotopes, Catheterization, Fasting, Glucagon, Gluconeogenesis, Insulin, Intestinal Mucosa, Liver, Tritium
Show Abstract · Added December 10, 2013
The complexity of the process of gluconeogenesis makes it very difficult to study in vivo. Of the many approaches used to study this process, none have proven ideal. The arterial-hepatic venous catheterization technique can provide accurate determination of the net splanchnic uptake of the various gluconeogenic precursors but gives no information as to their fate once extracted. The infusion of a labeled precursor, such as [14C]alanine, will provide qualitative information about the fate of the labeled substrate but, without complicated kinetic analysis, will not provide quantitative information on the conversion of the precursor to glucose. Though each of these individual techniques has major limitations in the study of gluconeogenesis, various combinations of these methods can provide further insight into the regulation of this complicated process. By combining the arterial-hepatic venous catheterization technique with the infusion of a labeled precursor, the splanchnic extraction of the precursor can be measured as well as the amount of the extracted precursor that is converted to glucose. The concomitant infusion of two isotopes (a 14C-labeled gluconeogenic precursor to assess substrate conversion to glucose and 3H-labeled glucose to measure glucose turnover) can also provide an accurate determination of the amount of circulating precursor that is converted to glucose. The latter technique provides no information on the splanchnic extraction of the precursor but has the advantage of being less invasive and, therefore, more applicable to man. The last two techniques measure accurately the direct conversion of the circulating precursor to glucose and, therefore, provide reliable index of gluconeogenesis.
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13 MeSH Terms
[Replacement of saccharose with other sweetening agents and their effect on experimental caries in rats].
KurhaĊ„ska A, Buchowski M, Gawecki J
(1979) Czas Stomatol 32: 143-8
MeSH Terms: Animals, Cariogenic Agents, Dental Caries, Glucose, Glycine, Rats, Sorbitol, Sucrose, Sweetening Agents
Added July 31, 2015
0 Communities
1 Members
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9 MeSH Terms
The effect of somatostatin on glucose uptake and production by rat tissues in vitro.
Cherrington AD, Caldwell MD, Dietz MR, Exton JH, Crofford OB
(1977) Diabetes 26: 740-8
MeSH Terms: Adipose Tissue, Animals, Cyclic AMP, Dose-Response Relationship, Drug, Glucagon, Glucose, Hindlimb, In Vitro Techniques, Insulin, Liver, Male, Muscles, Protein Kinases, Rats, Somatostatin
Added December 10, 2013
0 Communities
1 Members
0 Resources
15 MeSH Terms