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1 of glucose-6-phosphatase resulting in severe fasting hypoglycemia.
2 interference (RNAi) to the liver, experience fasting hypoglycemia.
3  and fasting conditions was achieved without fasting hypoglycemia.
4 as a result, CD36Tg mice were protected from fasting hypoglycemia.
5        At baseline, Arrdc4-KO mice have mild fasting hypoglycemia.
6 paired glucose homeostasis and a hallmark of fasting hypoglycemia.
7 ion suppresses gluconeogenesis, resulting in fasting hypoglycemia.
8    In parallel, the VAMP8 null mice also had fasting hypoglycemia (84 +/- 11 vs. 115 +/- 4) and enhan
9                       They also have chronic fasting hypoglycemia and a reduced rise in blood glucose
10 dren with unexplained, recurrent, and severe fasting hypoglycemia and asymmetrical growth.
11  selective SST5 agonist effectively prevents fasting hypoglycemia and suppresses insulin secretion no
12 is primarily a hyperglycemic agent driven by fasting/hypoglycemia and highlight the recent advances t
13  As in the humans with HI/HA, H454Y mice had fasting hypoglycemia, but plasma insulin concentrations
14 ntly increased fasting glucose and prevented fasting hypoglycemia compared to vehicle in Sur1(-/-) mi
15                Metabolic evaluation revealed fasting hypoglycemia, dicarboxylic aciduria, and reduced
16 up to 98% and resulted in failure to thrive, fasting hypoglycemia, hypertriglyceridemia, hepatomegaly
17 henotypes in terms of hepatic G6PC activity, fasting hypoglycemia, hypertriglyceridemia, hepatomegaly
18                                          The fasting hypoglycemia in Foxa3(-/-) mice could not be att
19                                 Pathological fasting hypoglycemia in humans is usually explained by e
20 ings indicate that exendin-(9-39) normalizes fasting hypoglycemia in SUR-1(-/-) mice via a direct eff
21 9) suppresses insulin secretion and corrects fasting hypoglycemia in SUR-1(-/-) mice.
22 blation of FoxO genes causes more pronounced fasting hypoglycemia, increased glucose tolerance, and e
23 s characterized by reduced glycogen storage, fasting hypoglycemia, increased insulin sensitivity and
24 y insensitive to glucocorticoids, exhibiting fasting hypoglycemia, increased insulin sensitivity desp
25 DH sensitivity to GTP inhibition, leading to fasting hypoglycemia, leucine hypersensitivity, and prot
26                               The finding of fasting hypoglycemia raises important clinical questions
27          Acute ethanol intoxication promotes fasting hypoglycemia through an increase in hepatic NADH
28 terregulatory hormone to insulin, induced by fasting/hypoglycemia to raise blood glucose through acti
29                                              Fasting hypoglycemia was associated with normal levels o