ライフサイエンスコーパス: hyperglucagonemia

1 ta-cell mass, increased alpha-cell mass, and hyperglucagonemia.

2 ls adopted the alpha cell fate, resulting in hyperglucagonemia.

3 ncreas with anti-insulin serum causes marked hyperglucagonemia.

4 s the catabolic state through suppression of hyperglucagonemia.

5 and increased relative alpha-cell volume and hyperglucagonemia.

6 tic and extrahepatic insulin resistance, and hyperglucagonemia.

7 the hypocholesterolemia is secondary to the hyperglucagonemia.

8 an increase in the direct insulin effect at hyperglucagonemia.

9 d did not improve hyperglycemia in mice with hyperglucagonemia.

10 There was marked alpha-cell hyperplasia and hyperglucagonemia (~1,200 pg/mL), but hepatic phosphoryl

11 , which was surprisingly not associated with hyperglucagonemia, a typical manifestation in T1D.

12 e tolerance test and suppressed postprandial hyperglucagonemia after mixed meal tolerance test.

13 Because diabetic patients often have hyperglucagonemia, AMPKalpha phosphorylation at Ser-485/

14 cgr signaling, Gcgr(Hep)(-/-) mice developed hyperglucagonemia and alpha-cell hyperplasia.

15 gptl4) links glucagon receptor inhibition to hyperglucagonemia and alpha-cell proliferation.

16 was associated with expected correction from hyperglucagonemia and hyperphagia.

17 sion may thus ameliorate the consequences of hyperglucagonemia and improve blood glucose control in d

18 Glucagon-like peptide 1 (GLP-1) reduces hyperglucagonemia and postprandial TRL, the latter in pa

19 ibition of gluconeogenesis by suppression of hyperglucagonemia and reduction of hepatic cAMP response

20 the MMT as the combined result of a relative hyperglucagonemia and the rapid fall in plasma glucose a

21 Hyperglucagonemia and/or an elevated glucagon-to-insulin

22 and then to extrahepatic insulin resistance, hyperglucagonemia, and diabetes.

23 and ameliorated hepatic insulin resistance, hyperglucagonemia, and dyslipidemia.

24 ion between protein catabolic conditions and hyperglucagonemia, and enhanced glucagon secretion by am

25 hese SMA mice display fasting hyperglycemia, hyperglucagonemia, and glucose resistance.

26 Early-stage type 1 diabetes (T1D) exhibits hyperglucagonemia by undefined cellular mechanisms.

27 nts with type 2 diabetes (T2D) often exhibit hyperglucagonemia despite hyperglycemia, implicating def

28 Hyperglucagonemia did not affect leucine transamination.

29 We studied the effects of hyperglucagonemia during insulin deprivation on energy e

30 n, T2D hyperglycemia requires unsuppressible hyperglucagonemia from insulin-resistant alpha cells and

31 ieved to be a pancreas-specific hormone, and hyperglucagonemia has been shown to contribute significa

32 This hyperglucagonemia has been thought to arise from alpha-c

33 The direct effect increases with hyperglucagonemia; however, the indirect effect remains

34 Mice treated with low-dose STZ exhibited hyperglucagonemia, hyperglycemia, and glucose intoleranc

35 gulatory defects including hyperinsulinemia, hyperglucagonemia, hyperglycemia, and insulin resistance

36 ethality and greatly improves hyperglycemia, hyperglucagonemia, hyperketonemia, and polyuria caused b

37 Hyperglucagonemia in STZ-induced diabetes is thus likely

38 e gastrointestinal tract elicits significant hyperglucagonemia in these patients.

39 It is possible that postprandial hyperglucagonemia in type 2 diabetes is due to impaired

40 We conclude that postprandial hyperglucagonemia in type 2 diabetes is likely due to lo

41 ced glucose-stimulated insulin secretion and hyperglucagonemia, in addition to changes in islet compo

42 type 1 and type 2 diabetes because unopposed hyperglucagonemia is a pertinent contributor to diabetic

43 Hyperglucagonemia is implicated in the etiology of this

44 in action on euglycemia restoration and that hyperglucagonemia is not required for T1D.

45 features present in insulin deficiency; (b) hyperglucagonemia is present in every form of poorly con

46 ulin deficiency increases protein breakdown, hyperglucagonemia is primarily responsible for the incre

47 nsulin-deficient diabetes (uDM), but whether hyperglucagonemia is required for hyperglycemia in this

48 These data suggest that in rats with uDM, hyperglucagonemia is required for ketosis but not for in

49 These findings lead us to propose that hyperglucagonemia may additionally aggravate the diabeti

50 a1 expression on alpha-cells may explain the hyperglucagonemia observed in prediabetic NOD mice and m

51 ns, but whether these effects persist during hyperglucagonemia of longer duration is unclear.

52 timulation of EE and HGP is sustained during hyperglucagonemia of longer duration when insulin secret

53 glucagon receptor inhibition to compensatory hyperglucagonemia or expansion of alpha-cell mass, and t

54 tide in a dose-escalating regimen to reverse hyperglucagonemia or its vehicle for 10 days.

55 Prediabetic NOD mice exhibit hyperglucagonemia, possibly due to an intrinsic alpha-ce

56 We hypothesize that the hyperglucagonemia prevents hypoglycemia and that the hyp

57 We hypothesized that postabsorptive hyperglucagonemia represents a gut-dependent phenomenon

58 The resulting hyperglucagonemia stimulates hepatic glucose production,

59 Hyperglucagonemia was also associated with a trend for d

60 However, the role of hyperglucagonemia, which occurs concomitantly with insul