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1 ypoglycemia produced a threefold increase in plasma glucagon.
2 ively, P < 0.05 for both) and no increase in plasma glucagon.
3 increased ( approximately 10-fold) levels of plasma glucagon.
4 nd yet associates with dramatic increases in plasma glucagon.
5 ever, produced a more pronounced blunting of plasma glucagon, ACTH, and hepatic glucose production co
7 as associated with a significant increase in plasma glucagon and a decrease in the plasma insulin con
8 ng antibody to healthy individuals increased plasma glucagon and amino acid levels, but did not chang
9 sociated with decreased food intake, reduced plasma glucagon and corticosterone concentrations, and d
10 only slightly, it fully normalized elevated plasma glucagon and corticosterone levels and reversed t
11 ose, plasma lipids, liver triglycerides, and plasma glucagon and enhanced pancreatic insulin content,
15 -/-) mice have elevated ( approximately 60%) plasma glucagon and reduced ( approximately 20%) plasma
16 lucose and was accompanied by lowered HbA1c, plasma glucagon, and triglyceride concentrations and exp
17 stion resulted in elevated serum insulin and plasma glucagon compared with FRU and MF (P < 0.001 for
18 fatty acid was accompanied by a fall in the plasma glucagon concentration from 122 to 85 pmol/L (P =
20 results in higher plasma glucose and higher plasma glucagon concentrations after a mixed meal and af
21 sfunction, characterized by elevated fasting plasma glucagon concentrations and inadequate postprandi
22 In humans, postprandial lipemia increased plasma glucagon concentrations and led to an inadequate
24 and mice, chronic physiological increases in plasma glucagon concentrations increased mitochondrial o
25 gon was infused at rates designed to achieve plasma glucagon concentrations spanning the physiologica
28 fusion (4 ng/kg/min), achieving steady-state plasma glucagon concentrations, followed by a 1-hour was
31 hours and were independent of any changes in plasma glucagon concentrations; these effects were abrog
33 nd the hepatic portal-arterial difference in plasma glucagon decreased slightly from 41 +/- 7 and 4 +
34 whether macronutrient infusion can suppress plasma glucagon during critical illness and study the ro
36 In patients with diabetes, elevations in plasma glucagon, epinephrine, and norepinephrine were bl
37 /- 6 pM), suppression of glucagon secretion (plasma glucagon, I:31 +/- 4, II: 63 +/- 8 pg/ml) doubled
38 nd the hepatic portal-arterial difference in plasma glucagon increased from 43 +/- 5 and 4 +/- 2 to 5
41 tor monoclonal antibody undergo elevation of plasma glucagon levels and alpha-cell expansion similar
42 effect associated with normalization of both plasma glucagon levels and hepatic expression of glucone
44 plus xenin-25 transiently increased ISR and plasma glucagon levels in subjects with NGT and IGT but
47 were associated with protein breakdown, and plasma glucagon levels were inversely correlated with pr
56 sulin secretion (P < .01), and 3-fold larger plasma glucagon-like peptide-1(7-36) (GLP-1(7-36)) excur
57 nd the hepatic portal-arterial difference in plasma glucagon (ng/l) did not change significantly (43
58 nd the hepatic portal-arterial difference in plasma glucagon (ng/l) did not rise significantly (40 +/
59 nd the hepatic portal-arterial difference in plasma glucagon (ng/l) rose from 43 +/- 5 and 5 +/- 2 to
60 content, increased proinsulin, and augmented plasma glucagon observed in KATP-GOF mice were normalize
61 n EGP cannot be explained by the increase in plasma glucagon or decrease in plasma insulin or glucose
63 tradiol also attenuated hypoglycemia-induced plasma glucagon, pituitary proopiomelanocortin (POMC), a
64 he great potential that normalization of the plasma glucagon profile may have for the treatment of T2
67 both FRU and MF (P < 0.05 for all), although plasma glucagon was also higher when compared with PRO (
71 ticosteroid levels were altered as expected, plasma glucagon was reduced markedly in the mutant anima