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1 rus-mediated expression of IL-10 ameliorates postprandial hyperglycemia.
2 ts on glucose absorption, in order to manage postprandial hyperglycemia.
3 n in type 2 diabetic patients and exacerbate postprandial hyperglycemia.
4 e -- that were fed a high-fat diet developed postprandial hyperglycemia.
5 lucose tolerance was normal, except for mild postprandial hyperglycemia.
6 on by enhancing glucoregulation and reducing postprandial hyperglycemia.
7 in insulin secretion is the primary cause of postprandial hyperglycemia.
8 glucose metabolism and is protective against postprandial hyperglycemia.
9  5-HT or 5-HT receptor agonists might reduce postprandial hyperglycemia.
10 the treated animals still exhibited moderate postprandial hyperglycemia.
11 tration, which may have contributed to their postprandial hyperglycemia.
12 ptake by muscle contribute almost equally to postprandial hyperglycemia.
13  it at greater risk for ROS damage caused by postprandial hyperglycemia.
14 esponsible for the enzyme inhibition against postprandial hyperglycemia.
15 easible strategy to reduce daily exposure to postprandial hyperglycemia.
16 s functional food ingredients for regulating postprandial hyperglycemia.
17 pring normalizes body temperature and causes postprandial hyperglycemia.
18                             As such, overall postprandial hyperglycemia (24-h incremental area under
19               The LCBF significantly reduced postprandial hyperglycemia after breakfast (P < 0.01) an
20 n nutraceutical ingredient, able to mitigate postprandial hyperglycemia and counteract the ROS overpr
21                                 Diet-induced postprandial hyperglycemia and fasting hyperinsulinemia
22 ewise, the molecular defects associated with postprandial hyperglycemia and impaired hepatic glucose
23 o be sufficient to lower overall exposure to postprandial hyperglycemia and improve glycemic variabil
24                                 As a result, postprandial hyperglycemia and insulin release by the pa
25 unts of fructose with a glucose load reduces postprandial hyperglycemia and the pancreatic beta-cell
26  muscle insulin resistance and the resulting postprandial hyperglycemia are hallmarks of non-insulin-
27                      Premeal insulin reduced postprandial hyperglycemia by 2-3 mmol/L compared with p
28 n of slowly absorbed isomaltulose attenuates postprandial hyperglycemia by reducing oral glucose appe
29 patterns of glucose variation, in particular postprandial hyperglycemia, contribute uniquely to an in
30                   This likely contributes to postprandial hyperglycemia during pregnancy, with potent
31 , the mechanism by which isomaltulose limits postprandial hyperglycemia has not been clarified.
32       However, mechanisms that contribute to postprandial hyperglycemia have not been identified.
33 iminary evidence of benefit for body weight, postprandial hyperglycemia, hyperinsulinemia, and other
34 as been shown to be associated with improved postprandial hyperglycemia in allele carriers of a loss-
35 ly demonstrated to contribute to fasting and postprandial hyperglycemia in both type 1 and type 2 dia
36 ses likely leads to the early development of postprandial hyperglycemia in CF.
37 tivity can offer facile routes to ameliorate postprandial hyperglycemia in diabetes via control of st
38 decrease in SGU in NIDDM might contribute to postprandial hyperglycemia in diabetic subjects.
39 e as a treatment for oxidative stress due to postprandial hyperglycemia in early T2D in humans.
40                             We conclude that postprandial hyperglycemia in individuals with early dia
41 ration as a potential factor contributing to postprandial hyperglycemia in non-insulin-dependent diab
42 er understanding of the cause of fasting and postprandial hyperglycemia in people with type 2 diabete
43 ucose metabolism are likely to contribute to postprandial hyperglycemia in people with type 2 diabete
44 hyperglycemic activity against sugar-induced postprandial hyperglycemia in rats plausibly due to the
45 hyperglycemic activity against sugar-induced postprandial hyperglycemia in rats plausibly due to the
46                   A key strategy to mitigate postprandial hyperglycemia involves inhibiting alpha-amy
47                                              Postprandial hyperglycemia is an early indicator of abno
48                                              Postprandial hyperglycemia is associated with platelet a
49 patic gluconeogenesis, promoting fasting and postprandial hyperglycemia through increased fatty acid
50 ly permits a transient and optimal degree of postprandial hyperglycemia to efficiently enhance insuli
51 emia and glycemia after correcting excessive postprandial hyperglycemia using treatment with a sodium