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1 diabetes with insulitis, hyperglycemia, and hypoinsulinemia.
2 g, deficits in DAT function that result from hypoinsulinemia.
3 eks, mice on HFD exhibited hyperglycemia and hypoinsulinemia.
4 tal diabetes, evidenced by hyperglycemia and hypoinsulinemia.
5 demia, hepatic steatosis, hyperglycemia, and hypoinsulinemia.
6 alformations, impaired glucose tolerance and hypoinsulinemia.
7 ult mouse beta-cell caused hyperglycemia and hypoinsulinemia.
8 In HNF1A mutation carriers, we observed: 1) hypoinsulinemia, 2) insulinotropic effects of both GIP a
9 topic p53 gene encoding Delta40p53 developed hypoinsulinemia and glucose intolerance by 3 months of a
11 glycemia and glucose intolerance with severe hypoinsulinemia and reduced islet insulin content and gl
12 body weight, caused fetal hyperglycemia and hypoinsulinemia, and decreased the relative islet area.
13 e glucose control due to insulin resistance, hypoinsulinemia, and deteriorating pancreatic beta-cell
14 eonates presented with severe hyperglycemia, hypoinsulinemia, and drastically reduced hormone express
19 e literature on the effect of hyperglycemia, hypoinsulinemia, and ketoacidosis, as well as the role o
20 l fat deposition, and induced hyperglycemia, hypoinsulinemia, and low-density lipoprotein hypercholes
21 ad reduced beta-cell proliferation and mass, hypoinsulinemia, and mild diabetes, phenotypes rescued b
22 isplayed higher blood glucose levels, marked hypoinsulinemia, and reduced beta-cell mass compared wit
24 ocol I, hyperglycemic (approximately 10 mM) -hypoinsulinemia (approximately 40 pM); protocol II, eugl
25 breakdown, an acute gluconeogenic effect of hypoinsulinemia becomes manifest, whereas inhibition of
26 he severe hyperglycemia, diabetes incidence, hypoinsulinemia, beta-cell death, and loss of beta-cell
27 ssue, hypoadiponectinemia, hypoglycemia, and hypoinsulinemia but with relatively normal glucose dispo
29 pha deletion, mice develop hyperglycemia and hypoinsulinemia, due to defective beta cell function tha
30 stricted feeding (RF), immediately creates a hypoinsulinemia during the active phase, which initiates
31 eome of 120-d-old OVE26 transgenic mice with hypoinsulinemia, hyperglycemia, hyperlipidemia, and prot
32 lpha(-/-) mice, the p85beta(-/-) mice showed hypoinsulinemia, hypoglycemia, and improved insulin sens
33 We show that Asna1(beta-/-) mice develop hypoinsulinemia, impaired insulin secretion, and glucose
36 ts demonstrate that hyperglucagonemia during hypoinsulinemia increases net muscle protein catabolism
37 n both the streptozotocin (STZ) model, where hypoinsulinemia is chemically induced, and in the Ins2Ak
39 ensitivity of a brain reward system and that hypoinsulinemia may be the common factor in food restric
40 of a euglycemic clamp study, indicating that hypoinsulinemia promotes insulin sensitivity in chronica
41 in-induced hyperglycemia, which results from hypoinsulinemia, reduced expression of renal insulin rec
42 -AL, ALS/Lt mice exhibited hyperglycemia and hypoinsulinemia, whereas ALR/Lt mice maintained normal p