Genomics, Type 2 Diabetes, and Obesity  

Oleh:

McCarthy, Mark I.

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: The New England Journal of Medicine (keterangan: ada di Proquest) vol. 363 no. 24 (Dec. 2010), page 2339-2350.
Topik: DIABETES; Obesity
Fulltext: Intravitreal Triamcinolone.pdf (78.44KB)

Ketersediaan

Perpustakaan FK Nomor Panggil: N08.K.2010.01 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

Type 2 diabetes, though poorly understood, is known to be a disease characterized by an inadequate beta-cell response to the progressive insulin resistance that typically accompanies advancing age, inactivity, and weight gain.1 The disease accounts for substantial morbidity and mortality from adverse effects on cardiovascular risk and disease-specific complications such as blindness and renal failure.2 The increasing global prevalence of type 2 diabetes is tied to rising rates of obesity2 — in part a consequence of social trends toward higher energy intake and reduced energy expenditure. However, the mechanisms that underlie individual differences in the predisposition to obesity remain obscure. Failure to understand the pathophysiology of diseases such as type 2 diabetes and obesity frustrates efforts to develop improved therapeutic and preventive strategies. The identification of DNA variants influencing disease predisposition will, it is hoped, deliver clues to the processes involved in disease pathogenesis. This would not only spur translational innovation but also provide opportunities for personalized medicine through stratification according to an individual person's risk and more precise classification of the disease subtype. In this article, I consider the extent to which these objectives have been realized.

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