 |
|
Insulin Therapy and Lipid Overload in Type 2 Diabetes
|
|
| Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings. |
|
|
|
To the Editor: In his Commentary, Dr Unger1 raises many important issues regarding the pathophysiology of type 2 diabetes mellitus based on epidemiological, clinical, metabolic, and molecular information. His lipocentric schema is consistent with the known effects of overnutrition on insulin secretion, as well as the effects of insulin on the disposition of unused calories: initially as fat in adipocytes but ultimately as ectopic fat in nonadipocytes, such as beta cells and myocytes.1
It is possible that myocardial fat accumulation also contributes to diabetic cardiac complications. Inherited and acquired cardiomyopathies, such as those related to impaired glucose tolerance and diabetes, are associated with marked intracellular lipid accumulation in the heart.2 According to the pathway proposed by Unger,1 SREBP-1c is a transcription factor that controls lipogenesis and is induced during overnutrition to facilitate the conversion of glucose to fatty acids and triglycerides for the storage of the excess energy.3 Uncontrolled activation . . . [Full Text of this Article]
Raffaele Marfella, MD, PhD
raffaele.marfella@unina2.it
Michelangela Barbieri, MD, PhD;
Giuseppe Paolisso, MD
Department of Geriatrics and Metabolic Diseases
Second University of Naples
Naples, Italy
RELATED ARTICLE
Reinventing Type 2 Diabetes: Pathogenesis, Treatment, and Prevention
Roger H. Unger
JAMA. 2008;299(10):1185-1187.
EXTRACT
| FULL TEXT
RELATED LETTERS
Insulin Therapy and Lipid Overload in Type 2 Diabetes
Paresh Dandona, Ajay Chaudhuri, and Husam Ghanim
JAMA. 2008;300(7):788-789.
EXTRACT
| FULL TEXT
Insulin Therapy and Lipid Overload in Type 2 Diabetes—Reply
Roger H. Unger
JAMA. 2008;300(7):790.
EXTRACT
| FULL TEXT
|
