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1 etabolism and lead to hyperaminoacidemia and hyperglucagonemia.
2 ed glucose-stimulated insulin secretion, and hyperglucagonemia.
3 ikely explanation for fatty liver-associated hyperglucagonemia.
4 dysfunction consequent to GIP resistance and hyperglucagonemia.
5 to promote ketoacidosis are independent from hyperglucagonemia.
6 d did not improve hyperglycemia in mice with hyperglucagonemia.
7 ta-cell mass, increased alpha-cell mass, and hyperglucagonemia.
8 ls adopted the alpha cell fate, resulting in hyperglucagonemia.
9 ncreas with anti-insulin serum causes marked hyperglucagonemia.
10 s the catabolic state through suppression of hyperglucagonemia.
11 and increased relative alpha-cell volume and hyperglucagonemia.
12 tic and extrahepatic insulin resistance, and hyperglucagonemia.
13  the hypocholesterolemia is secondary to the hyperglucagonemia.
14  an increase in the direct insulin effect at hyperglucagonemia.
15  the diabetogenic effect of NAFLD-associated hyperglucagonemia.
16  There was marked alpha-cell hyperplasia and hyperglucagonemia (~1,200 pg/mL), but hepatic phosphoryl
17 , which was surprisingly not associated with hyperglucagonemia, a typical manifestation in T1D.
18 e tolerance test and suppressed postprandial hyperglucagonemia after mixed meal tolerance test.
19         Because diabetic patients often have hyperglucagonemia, AMPKalpha phosphorylation at Ser-485/
20 ing lowers blood glucose but also results in hyperglucagonemia and alpha-cell hyperplasia.
21 cgr signaling, Gcgr(Hep)(-/-) mice developed hyperglucagonemia and alpha-cell hyperplasia.
22 gptl4) links glucagon receptor inhibition to hyperglucagonemia and alpha-cell proliferation.
23 plain why patients with type 2 diabetes have hyperglucagonemia and how NAFLD disrupts the liver-alpha
24 was associated with expected correction from hyperglucagonemia and hyperphagia.
25 sion may thus ameliorate the consequences of hyperglucagonemia and improve blood glucose control in d
26                        She was found to have hyperglucagonemia and pancreatic hypertrophy with geneti
27      Glucagon-like peptide 1 (GLP-1) reduces hyperglucagonemia and postprandial TRL, the latter in pa
28 ibition of gluconeogenesis by suppression of hyperglucagonemia and reduction of hepatic cAMP response
29 hese drugs cause euglycemic ketoacidosis and hyperglucagonemia and stimulate hepatic gluconeogenesis
30 the MMT as the combined result of a relative hyperglucagonemia and the rapid fall in plasma glucose a
31                                              Hyperglucagonemia and/or an elevated glucagon-to-insulin
32 ce, however patients with diabetes exhibited hyperglucagonemia, and compromised beta-cell function de
33 and then to extrahepatic insulin resistance, hyperglucagonemia, and diabetes.
34  and ameliorated hepatic insulin resistance, hyperglucagonemia, and dyslipidemia.
35 ion between protein catabolic conditions and hyperglucagonemia, and enhanced glucagon secretion by am
36 hese SMA mice display fasting hyperglycemia, hyperglucagonemia, and glucose resistance.
37  effects, such as alpha-cell hyperplasia and hyperglucagonemia, and the mechanisms underlying these s
38 roximately sixfold basal), and unprecedented hyperglucagonemia (approximately eightfold basal) while
39 C1 signaling is sufficient to induce chronic hyperglucagonemia as a result of a-cell proliferation, c
40 C1 signaling is sufficient to induce chronic hyperglucagonemia as a result of alpha-cell proliferatio
41 PNS had no effect on the RaO or meal-induced hyperglucagonemia but increased EGP in SG without any ef
42   Early-stage type 1 diabetes (T1D) exhibits hyperglucagonemia by undefined cellular mechanisms.
43       These studies demonstrate that chronic hyperglucagonemia can improve glucose homeostasis by ind
44  not suppress EGP, and 3) that physiological hyperglucagonemia can override the hepatic actions of in
45                                              Hyperglucagonemia contributes to hyperglycemia in patien
46 nts with type 2 diabetes (T2D) often exhibit hyperglucagonemia despite hyperglycemia, implicating def
47                                              Hyperglucagonemia did not affect leucine transamination.
48               These results demonstrate that hyperglucagonemia during hypoinsulinemia increases net m
49                    We studied the effects of hyperglucagonemia during insulin deprivation on energy e
50                             Despite prandial hyperglucagonemia, endogenous glucose production respons
51 n, T2D hyperglycemia requires unsuppressible hyperglucagonemia from insulin-resistant alpha cells and
52 ieved to be a pancreas-specific hormone, and hyperglucagonemia has been shown to contribute significa
53                                         This hyperglucagonemia has been thought to arise from alpha-c
54             The direct effect increases with hyperglucagonemia; however, the indirect effect remains
55      This group was characterized by fasting hyperglucagonemia, hyperaminoacidemia, and no lowering o
56 order of glucagon signaling characterized by hyperglucagonemia, hyperaminoacidemia, and pancreatic al
57     Mice treated with low-dose STZ exhibited hyperglucagonemia, hyperglycemia, and glucose intoleranc
58 gulatory defects including hyperinsulinemia, hyperglucagonemia, hyperglycemia, and insulin resistance
59 ethality and greatly improves hyperglycemia, hyperglucagonemia, hyperketonemia, and polyuria caused b
60                                              Hyperglucagonemia in alphaTSC2(KO) was associated with a
61                                              Hyperglucagonemia in aTSC2(KO) was associated with an in
62  on glucagon secretion may contribute to the hyperglucagonemia in diabetes and influence the success
63  parts of the molecular mechanism underlying hyperglucagonemia in GCGR blockade.
64                                              Hyperglucagonemia in STZ-induced diabetes is thus likely
65 e gastrointestinal tract elicits significant hyperglucagonemia in these patients.
66 kinetics of glucagon could contribute to the hyperglucagonemia in type 2 diabetes and obesity.
67             It is possible that postprandial hyperglucagonemia in type 2 diabetes is due to impaired
68                We conclude that postprandial hyperglucagonemia in type 2 diabetes is likely due to lo
69 ced glucose-stimulated insulin secretion and hyperglucagonemia, in addition to changes in islet compo
70 nsulin action and metabolism were altered by hyperglucagonemia including increase in branched-chain A
71 ransient insulin deprivation with concurrent hyperglucagonemia is a catabolic state that can occur in
72                                              Hyperglucagonemia is a common observation in both obesit
73 type 1 and type 2 diabetes because unopposed hyperglucagonemia is a pertinent contributor to diabetic
74                                              Hyperglucagonemia is a well-known contributor to diabeti
75                                              Hyperglucagonemia is implicated in the etiology of this
76 in action on euglycemia restoration and that hyperglucagonemia is not required for T1D.
77 naling increases hepatic glucose output, and hyperglucagonemia is partly responsible for the hypergly
78  features present in insulin deficiency; (b) hyperglucagonemia is present in every form of poorly con
79 ulin deficiency increases protein breakdown, hyperglucagonemia is primarily responsible for the incre
80 nsulin-deficient diabetes (uDM), but whether hyperglucagonemia is required for hyperglycemia in this
81    These data suggest that in rats with uDM, hyperglucagonemia is required for ketosis but not for in
82       These findings lead us to propose that hyperglucagonemia may additionally aggravate the diabeti
83 mination of glucagon could contribute to the hyperglucagonemia observed in chronic liver disease and
84 tion of the axis in humans may result in the hyperglucagonemia observed in diabetes.
85 n clearance is not a fundamental part of the hyperglucagonemia observed in obesity and type 2 diabete
86 a1 expression on alpha-cells may explain the hyperglucagonemia observed in prediabetic NOD mice and m
87 ns, but whether these effects persist during hyperglucagonemia of longer duration is unclear.
88 timulation of EE and HGP is sustained during hyperglucagonemia of longer duration when insulin secret
89 llowed us to identify the effects of chronic hyperglucagonemia on glucose homeostasis by inducing ins
90 glucagon receptor inhibition to compensatory hyperglucagonemia or expansion of alpha-cell mass, and t
91 tide in a dose-escalating regimen to reverse hyperglucagonemia or its vehicle for 10 days.
92                 Prediabetic NOD mice exhibit hyperglucagonemia, possibly due to an intrinsic alpha-ce
93                      We hypothesize that the hyperglucagonemia prevents hypoglycemia and that the hyp
94         Increased plasma levels of glucagon (hyperglucagonemia) promote diabetes development but are
95          We hypothesized that postabsorptive hyperglucagonemia represents a gut-dependent phenomenon
96                                The resulting hyperglucagonemia stimulates hepatic glucose production,
97                                              Hyperglucagonemia was also associated with a trend for d
98      High-fat diet-fed GC-/- mice have basal hyperglucagonemia, which is associated with decreased al
99                         However, the role of hyperglucagonemia, which occurs concomitantly with insul