ライフサイエンスコーパス: postprandial hyperglycemia

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1 s functional food ingredients for regulating postprandial hyperglycemia.

2 pring normalizes body temperature and causes 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 ts on glucose absorption, in order to manage postprandial hyperglycemia.

14 Diet-induced postprandial hyperglycemia and fasting hyperinsulinemia

15 ewise, the molecular defects associated with postprandial hyperglycemia and impaired hepatic glucose

16 As a result, postprandial hyperglycemia and insulin release by the pa

17 unts of fructose with a glucose load reduces postprandial hyperglycemia and the pancreatic beta-cell

18 muscle insulin resistance and the resulting postprandial hyperglycemia are hallmarks of non-insulin-

19 Premeal insulin reduced postprandial hyperglycemia by 2-3 mmol/L compared with p

20 n of slowly absorbed isomaltulose attenuates postprandial hyperglycemia by reducing oral glucose appe

21 patterns of glucose variation, in particular postprandial hyperglycemia, contribute uniquely to an in

22 This likely contributes to postprandial hyperglycemia during pregnancy, with potent

23 , the mechanism by which isomaltulose limits postprandial hyperglycemia has not been clarified.

24 However, mechanisms that contribute to postprandial hyperglycemia have not been identified.

25 ses likely leads to the early development of postprandial hyperglycemia in CF.

26 decrease in SGU in NIDDM might contribute to postprandial hyperglycemia in diabetic subjects.

27 We conclude that postprandial hyperglycemia in individuals with early dia

28 ration as a potential factor contributing to postprandial hyperglycemia in non-insulin-dependent diab

29 er understanding of the cause of fasting and postprandial hyperglycemia in people with type 2 diabete

30 ucose metabolism are likely to contribute to postprandial hyperglycemia in people with type 2 diabete

31 Postprandial hyperglycemia is an early indicator of abno

32 Postprandial hyperglycemia is associated with platelet a

33 patic gluconeogenesis, promoting fasting and postprandial hyperglycemia through increased fatty acid

34 ly permits a transient and optimal degree of postprandial hyperglycemia to efficiently enhance insuli

35 emia and glycemia after correcting excessive postprandial hyperglycemia using treatment with a sodium

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