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Fastic (Nateglinide)
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Nateglinide

Single-dose pharmacokinetics of Fastic in subjects with hepatic cirrhosis. The aim of this study is to evaluate the effect of Fastic on the insulin secretion at two different concentrations of glucose level. Fastic in combination with metformin in Chinese patients with type 2 diabetes mellitus: a post-marketing surveillance study.

Other names for this medication:
Nateglinide, Starlix, Fastic, Glinate, Incuria, Meglitinide, Starform, Starsis,

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Fastic is used to treat a type of diabetes mellitus (sugar diabetes) called type 2 diabetes. With this type of diabetes, insulin produced by the pancreas is not able to get sugar into the cells of the body where it can work properly. Using Fastic alone, or with metformin or a thiazolidinedione (other types of oral antidiabetic medicines), will help to lower blood sugar when it is too high and help restore the way you use food to make energy.

Many people can control type 2 diabetes with diet alone or with diet and exercise. Following a specially planned diet and exercising will always be important when you have diabetes, even when you are taking medicines. To work properly, the amount of Fastic you take must be balanced against the amount and type of food you eat and the amount of exercise you do. If you change your diet, your exercise, or both, you will want to test your blood sugar to find out if it is too low. Your health care professional will teach you what to do if this happens.

Fastic does not help patients who have insulin-dependent or type 1 diabetes because they cannot produce insulin from their pancreas gland. Their blood glucose is best controlled by insulin injections.

Fastic does not help patients who have already been treated with other antidiabetic medicines for a long time.

Fastic may be used together with metformin or a thiazolidinedione, but should not take the place of these medicines.

Fastic is available only with your doctor's prescription.

This product is available in the following dosage forms:

  • Tablet

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Effective management of acute myocardial infarction (AMI) is limited by patient delay in calling an ambulance. Sphingomyelin inhibited enzymatic activity and membrane-damaging activity of PLA(2) against egg yolk phosphatidylcholine (EYPC), while cholesterol and cholesterol sulfate abrogated the inhibitory effect of sphingomyelin. These results indicate that phenotypically heterogenous and penetrant cardiac malformations in Cited2 deficiency arise from a primary requirement in epiblast derivatives for left-right patterning, with a secondary cell-autonomous role in the mesoderm.

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