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Type 2 diabetes mellitus

DeFronzo, Ralph A. ; Ferrannini, Ele ; Groop, Leif LU ; Henry, Robert R. ; Herman, William H. ; Holst, Jens Juul ; Hu, Frank B. ; Kahn, C. Ronald ; Raz, Itamar and Shulman, Gerald I. , et al. (2015) In Nature Reviews Disease Primers 1.
Abstract

Type 2 diabetes mellitus (T2DM) is an expanding global health problem, closely linked to the epidemic of obesity. Individuals with T2DM are at high risk for both microvascular complications (including retinopathy, nephropathy and neuropathy) and macrovascular complications (such as cardiovascular comorbidities), owing to hyperglycaemia and individual components of the insulin resistance (metabolic) syndrome. Environmental factors (for example, obesity, an unhealthy diet and physical inactivity) and genetic factors contribute to the multiple pathophysiological disturbances that are responsible for impaired glucose homeostasis in T2DM. Insulin resistance and impaired insulin secretion remain the core defects in T2DM, but at least six... (More)

Type 2 diabetes mellitus (T2DM) is an expanding global health problem, closely linked to the epidemic of obesity. Individuals with T2DM are at high risk for both microvascular complications (including retinopathy, nephropathy and neuropathy) and macrovascular complications (such as cardiovascular comorbidities), owing to hyperglycaemia and individual components of the insulin resistance (metabolic) syndrome. Environmental factors (for example, obesity, an unhealthy diet and physical inactivity) and genetic factors contribute to the multiple pathophysiological disturbances that are responsible for impaired glucose homeostasis in T2DM. Insulin resistance and impaired insulin secretion remain the core defects in T2DM, but at least six other pathophysiological abnormalities contribute to the dysregulation of glucose metabolism. The multiple pathogenetic disturbances present in T2DM dictate that multiple antidiabetic agents, used in combination, will be required to maintain normoglycaemia. The treatment must not only be effective and safe but also improve the quality of life. Several novel medications are in development, but the greatest need is for agents that enhance insulin sensitivity, halt the progressive pancreatic β-cell failure that is characteristic of T2DM and prevent or reverse the microvascular complications. For an illustrated summary of this Primer, visit: http://go.nature.com/V2eGfN.

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publication status
published
subject
in
Nature Reviews Disease Primers
volume
1
article number
15019
publisher
Nature Publishing Group
external identifiers
  • scopus:84989193573
  • pmid:27189025
ISSN
2056-676X
DOI
10.1038/nrdp.2015.19
language
English
LU publication?
yes
id
c966e3c5-2b15-4955-a15d-c41a7f822e5b
date added to LUP
2019-02-01 15:03:36
date last changed
2024-04-15 22:51:42
@article{c966e3c5-2b15-4955-a15d-c41a7f822e5b,
  abstract     = {{<p>Type 2 diabetes mellitus (T2DM) is an expanding global health problem, closely linked to the epidemic of obesity. Individuals with T2DM are at high risk for both microvascular complications (including retinopathy, nephropathy and neuropathy) and macrovascular complications (such as cardiovascular comorbidities), owing to hyperglycaemia and individual components of the insulin resistance (metabolic) syndrome. Environmental factors (for example, obesity, an unhealthy diet and physical inactivity) and genetic factors contribute to the multiple pathophysiological disturbances that are responsible for impaired glucose homeostasis in T2DM. Insulin resistance and impaired insulin secretion remain the core defects in T2DM, but at least six other pathophysiological abnormalities contribute to the dysregulation of glucose metabolism. The multiple pathogenetic disturbances present in T2DM dictate that multiple antidiabetic agents, used in combination, will be required to maintain normoglycaemia. The treatment must not only be effective and safe but also improve the quality of life. Several novel medications are in development, but the greatest need is for agents that enhance insulin sensitivity, halt the progressive pancreatic β-cell failure that is characteristic of T2DM and prevent or reverse the microvascular complications. For an illustrated summary of this Primer, visit: http://go.nature.com/V2eGfN.</p>}},
  author       = {{DeFronzo, Ralph A. and Ferrannini, Ele and Groop, Leif and Henry, Robert R. and Herman, William H. and Holst, Jens Juul and Hu, Frank B. and Kahn, C. Ronald and Raz, Itamar and Shulman, Gerald I. and Simonson, Donald C. and Testa, Marcia A. and Weiss, Ram}},
  issn         = {{2056-676X}},
  language     = {{eng}},
  month        = {{07}},
  publisher    = {{Nature Publishing Group}},
  series       = {{Nature Reviews Disease Primers}},
  title        = {{Type 2 diabetes mellitus}},
  url          = {{http://dx.doi.org/10.1038/nrdp.2015.19}},
  doi          = {{10.1038/nrdp.2015.19}},
  volume       = {{1}},
  year         = {{2015}},
}