RSS Feeds
Intensive Therapy Preserves Insulin Secretion
The Editors welcome submissions for possible publication in the Letters section. Authors of letters should:
•Include no more than 300 words of text, three authors, and five references
•Type with double-spacing
•Send three copies of the letter, an authors' form signed by all authors, and a cover letter describing any conflicts of interest related to the contents of the letter.
Letters commenting on an Annals article will be considered if they are received within 6 weeks of the time the article was published. Only some of the letters received can be published. Published letters are edited and may be shortened; tables and figures are included only selectively. Authors will be notified that the letter has been received. If the letter is selected for publication, the author will be notified about 3 weeks before the publication date. Unpublished letters cannot be returned.
Annals welcomes electronically submitted letters.
TO THE EDITOR:
The most recent article by the DCCT Research Group [1] was intriguing and thought-provoking. I wish to hypothesize another potential benefit of sustaining islet-cell function apart from maintenance of C-peptide secretion. The hypothesis may also partially explain the better metabolic control and lower risk for hypoglycemia seen in the C-peptide responders.
Amylin (islet amyloid polypeptide) is normally co-secreted with insulin by pancreatic β cells [2]. It is reasonable to assume that preservation of β-cell function in patients with type 1 diabetes should not only permit a residual insulin (C-peptide) response but also maintain detectable plasma amylin levels, albeit low levels. Preserved amylin secretion would be expected to contribute to improved glycemic control by reducing postprandial hyperglycemic excursions through retarding gastric emptying and inhibiting amino acid-stimulated glucagon secretion [3].
Suppressed glucagon secretion may result in reduced postprandial hepatic glucose production but would not inhibit the counterregulatory glucagon response to hypoglycemia [4], thus reducing the risk for severe hypoglycemic events. The reduced incidence of hypoglycemia may also be due to residual amylin's effect of increasing plasma concentrations of growth hormone and cortisol and by the release of gluconeogenic substrates, such as lactate, from skeletal muscles [5]. In the fasting state, lactate may also help to replenish depleted glycogen stores.
I believe that these mechanisms warrant attention and would merit a reanalysis of any stored plasma samples from DCCT participants for the presence of physiologic levels of amylin.
Zeno L. Charles-Marcel, MD
Loma Linda University School of Medicine; Loma Linda, CA 92354
The Editors welcome submissions for possible publication in the Letters section. Authors of letters should:
•Include no more than 300 words of text, three authors, and five references
•Type with double-spacing
•Send three copies of the letter, an authors' form signed by all authors, and a cover letter describing any conflicts of interest related to the contents of the letter.
Letters commenting on an Annals article will be considered if they are received within 6 weeks of the time the article was published. Only some of the letters received can be published. Published letters are edited and may be shortened; tables and figures are included only selectively. Authors will be notified that the letter has been received. If the letter is selected for publication, the author will be notified about 3 weeks before the publication date. Unpublished letters cannot be returned.
Annals welcomes electronically submitted letters.
- Copyright ©2004 by the American College of Physicians
