Lessons Learned from Clinical and Basic Research Applied to the Study of Patients with Severe Insulin Resistance

Author(s):  
David E. Moller ◽  
Heike Benecke
Diabetes ◽  
1984 ◽  
Vol 33 (12) ◽  
pp. 1133-1137 ◽  
Author(s):  
B. R. Blazar ◽  
C. B. Whitley ◽  
A. E. Kitabchi ◽  
M. Y. Tsai ◽  
J. Santiago ◽  
...  

2019 ◽  
Vol 104 (11) ◽  
pp. 5372-5381 ◽  
Author(s):  
Nigel K Stepto ◽  
Alba Moreno-Asso ◽  
Luke C McIlvenna ◽  
Kirsty A Walters ◽  
Raymond J Rodgers

Abstract Context Polycystic ovary syndrome (PCOS) is a common endocrine condition affecting 8% to 13% of women across the lifespan. PCOS affects reproductive, metabolic, and mental health, generating a considerable health burden. Advances in treatment of women with PCOS has been hampered by evolving diagnostic criteria and poor recognition by clinicians. This has resulted in limited clinical and basic research. In this study, we provide insights into the current and future research on the metabolic features of PCOS, specifically as they relate to PCOS-specific insulin resistance (IR), that may affect the most metabolically active tissue, skeletal muscle. Current Knowledge PCOS is a highly heritable condition, yet it is phenotypically heterogeneous in both reproductive and metabolic features. Human studies thus far have not identified molecular mechanisms of PCOS-specific IR in skeletal muscle. However, recent research has provided new insights that implicate energy-sensing pathways regulated via epigenomic and resultant transcriptomic changes. Animal models, while in existence, have been underused in exploring molecular mechanisms of IR in PCOS and specifically in skeletal muscle. Future Directions Based on the latest evidence synthesis and technologies, researchers exploring molecular mechanisms of IR in PCOS, specifically in muscle, will likely need to generate new hypothesis to be tested in human and animal studies. Conclusion Investigations to elucidate the molecular mechanisms driving IR in PCOS are in their early stages, yet remarkable advances have been made in skeletal muscle. Overall, investigations have thus far created more questions than answers, which provide new opportunities to study complex endocrine conditions.


Diabetes ◽  
2017 ◽  
Vol 66 (10) ◽  
pp. 2713-2723 ◽  
Author(s):  
Jun Hosoe ◽  
Hiroko Kadowaki ◽  
Fuyuki Miya ◽  
Katsuya Aizu ◽  
Tomoyuki Kawamura ◽  
...  

10.1038/ng926 ◽  
2002 ◽  
Vol 31 (4) ◽  
pp. 379-384 ◽  
Author(s):  
David B. Savage ◽  
Maura Agostini ◽  
Inês Barroso ◽  
Mark Gurnell ◽  
Jian'an Luan ◽  
...  

1982 ◽  
Vol 243 (1) ◽  
pp. E15-E30 ◽  
Author(s):  
J. M. Olefsky ◽  
O. G. Kolterman ◽  
J. A. Scarlett

Resistance to the action of insulin can result from a variety of causes, including the formation of abnormal insulin or proinsulin molecules, the presence of circulating antagonists to insulin or the insulin receptor, or defects in insulin action at the target tissue level. Defects of the latter type are characteristic of obesity and of noninsulin-dependent diabetes mellitus. Analysis of the nature of the insulin resistance in those disorders has been investigated in intact subjects with the use of the euglycemic glucose clamp technique, and both insulin receptors and insulin-mediated glucose metabolism have been studied in adipocytes and monocytes from affected individuals. In both conditions, the cause of insulin resistance is heterogeneous. In some, insulin resistance appears to be due to a defect in the insulin receptor, whereas others have a defect both in the receptor and at the postreceptor level. In both groups, more severe insulin resistance is due to the postreceptor lesion and is correctable with appropriate therapy.


2017 ◽  
Vol 3 (1) ◽  
pp. e17-e21
Author(s):  
Raya A. Almazrouei ◽  
Juma Alkaabi ◽  
Fatima M. Alkaabi ◽  
Hanan Alshamsi

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