Type 2 diabetes: principles of pathogenesis and therapy
By M. Stumvoll, B. Goldstein, T. W. van Haeften. The Lancet, 2005
2,676 citations recorded by the source corpus.
Subfields: Epidemiology, Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/a812cb493f8dd2708d635dc2ce55617f7bbc5ee3
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Epidemiology
- A. Benito-Vicente
- A. Larrea-Sebal
- U. Galicia-Garcia
- M. Roden
- Philippe Froguel
- César Martín
- James B. Meigs
- F. B. Hu
In Molecular Biology
- Cristen J. Willer
- Yurii S. Aulchenko
- Gonçalo R. Abecasis
- R. Disanto
- Markku Laakso
- Mark J. Daly
- Leif Groop
- Zhen Gu
In Physiology
Citations in the corpus
- Horror autoinflammaticus: the molecular pathophysiology of autoinflammatory disease (*). (2009, background): “In contrast, type 2 diabetes mellitus (T2DM) tends to occur later in life and is due to the combination of peripheral insulin resistance and impaired islet cell insulin secretion, which are thought to be metabolic consequences of excessive weight (142).”
- Twelve type 2 diabetes susceptibility loci identified through large-scale association analysis (2010, background): “609" language="eng" relation="no"> Type 2 diabetes (T2D) is characterized by insulin resistance and deficient beta-cell functio”
- Therapeutic Potential of Moringa oleifera Leaves in Chronic Hyperglycemia and Dyslipidemia: A Review (2012, background): “Excess plasma NEFA impairs insulin secretion by β cells, stimulates gluconeogenesis by liver, and inhibits glucose disposal by skeletal muscle, further exacerbating hyperglycemia (Stumvoll et al., 2005).”
- Pathophysiology of Type 2 Diabetes Mellitus (2020, background): “Regarding the pathophysiology of the disease, a malfunctioning of the feedback loops between insulin action and insulin secretion results in abnormally high glucose levels in blood [2].”
- Antioxidants prevent health-promoting effects of physical exercise in humans (2009, background): “Type 2 diabetes mellitus is caused by a combination of insulin resistance involving a number of peripheral tissues, including skeletal muscle (2, 3), and an inadequate -cell response despite normal or even increased amounts of circulating insulin.”
- Large-scale association analysis provides insights into the genetic architecture and pathophysiology of type 2 diabetes (2012, neutral): “Type 2 diabetes (T2D) is a chronic metabolic disease with multifactorial pathogenesis 1 .”
- Microneedle-array patches loaded with hypoxia-sensitive vesicles provide fast glucose-responsive insulin delivery (2015, background): “Diabetes Res Clin Pract 28(2): 103–117.”
- An Expanded Genome-Wide Association Study of Type 2 Diabetes in Europeans (2017, neutral): “The development of T2D involves dysfunction of multiple mechanisms across several distinct tissues (9,29,31,47,48).”
- Adipose triglyceride lipase-mediated lipolysis of cellular fat stores is activated by CGI-58 and defective in Chanarin-Dorfman Syndrome. (2006, background): “The rate of FFA release from adipose tissue in humans and rodents is strongly associated with the development of insulin resistance and type 2 diabetes (Stumvoll et al., 2005), but the mechanisms and regulation of FFA release from stored fat remain insufficiently understood (Boden and Shulman, 2002;”