scholarly journals Publisher Correction: Central nervous system regulation of organismal energy and glucose homeostasis

2021 ◽  
Author(s):  
Martin G. Myers ◽  
Alison H. Affinati ◽  
Nicole Richardson ◽  
Michael W. Schwartz
2021 ◽  
Vol 3 (6) ◽  
pp. 737-750
Author(s):  
Martin G. Myers ◽  
Alison H. Refined ◽  
Nicole Richardson ◽  
Michael W. Schwartz

2012 ◽  
Vol 19 (2) ◽  
pp. 207-214 ◽  
Author(s):  
Cristina Muntean ◽  
Maria Mota ◽  
Simona Popa ◽  
Adina Mitrea

Abstract Central nervous system, mainly the hypothalamus and the brainstem are importantkeys in glucose homeostasis. Not only do they use glucose as primary fuel for theirfunctioning but they are part of intricate neuronal circuits involved in glucose uptakeand production as was first shown by Claude Bernard. Moreoverelectrophysiological analysis of hypothalamus revealed the existence of glucosensingneurons whose firing rates are controlled by glucose extracellular level. Furtherinformation was obtained regarding the importance of leptin, insulin and free fattyacids as afferent signals received by these neural structures. As for the main efferentpathways, autonomic system is the one connecting CNS with the effector organs (theliver, the pancreas and the adrenal glands).


Endocrinology ◽  
2017 ◽  
Vol 158 (7) ◽  
pp. 2124-2133 ◽  
Author(s):  
Lene Jessen ◽  
Eric P. Smith ◽  
Yvonne Ulrich-Lai ◽  
James P. Herman ◽  
Randy J. Seeley ◽  
...  

2008 ◽  
Vol 109 (1) ◽  
pp. 137-148 ◽  
Author(s):  
J A. Jeevendra Martyn ◽  
Masao Kaneki ◽  
Shingo Yasuhara ◽  
David S. Warner ◽  
Mark A. Warner

Obesity is a major cause of type 2 diabetes, clinically evidenced as hyperglycemia. The altered glucose homeostasis is caused by faulty signal transduction via the insulin signaling proteins, which results in decreased glucose uptake by the muscle, altered lipogenesis, and increased glucose output by the liver. The etiology of this derangement in insulin signaling is related to a chronic inflammatory state, leading to the induction of inducible nitric oxide synthase and release of high levels of nitric oxide and reactive nitrogen species, which together cause posttranslational modifications in the signaling proteins. There are substantial differences in the molecular mechanisms of insulin resistance in muscle versus liver. Hormones and cytokines from adipocytes can enhance or inhibit both glycemic sensing and insulin signaling. The role of the central nervous system in glucose homeostasis also has been established. Multipronged therapies aimed at rectifying obesity-induced anomalies in both central nervous system and peripheral tissues may prove to be beneficial.


Author(s):  
Zaman Mirzadeh ◽  
Chelsea L. Faber ◽  
Michael W. Schwartz

Historically, pancreatic islet beta cells have been viewed as principal regulators of glycemia, with type 2 diabetes (T2D) resulting when insulin secretion fails to compensate for peripheral tissue insulin resistance. However, glycemia is also regulated by insulin-independent mechanisms that are dysregulated in T2D. Based on evidence supporting its role both in adaptive coupling of insulin secretion to changes in insulin sensitivity and in the regulation of insulin-independent glucose disposal, the central nervous system (CNS) has emerged as a fundamental player in glucose homeostasis. Here, we review and expand upon an integrative model wherein the CNS, together with the islet, establishes and maintains the defended level of glycemia. We discuss the implications of this model for understanding both normal glucose homeostasis and T2D pathogenesis and highlight centrally targeted therapeutic approaches with the potential to restore normoglycemia to patients with T2D.


Sign in / Sign up

Export Citation Format

Share Document