Hyperactivity of the hypothalamic-pituitary-adrenal axis in patients with type 2 diabetes and relations with insulin resistance and chronic complications

2012 ◽  
Vol 124 (11-12) ◽  
pp. 403-411 ◽  
Author(s):  
Ivana Prpić-Križevac ◽  
Silvija Canecki-Varžić ◽  
Ines Bilić-Ćurčić
2007 ◽  
Vol 293 (5) ◽  
pp. E1451-E1458 ◽  
Author(s):  
Esben S. Buhl ◽  
Susanne Neschen ◽  
Shin Yonemitsu ◽  
Joerg Rossbacher ◽  
Dongyan Zhang ◽  
...  

Individuals born with a low birth weight (LBW) have an increased prevalence of type 2 diabetes, but the mechanisms responsible for this association are unknown. Given the important role of insulin resistance in the pathogenesis of type 2 diabetes, we examined insulin sensitivity in a rat model of LBW due to intrauterine fetal stress. During the last 7 days of gestation, rat dams were treated with dexamethasone and insulin sensitivity was assessed in the LBW offspring by a hyperinsulinemic euglycemic clamp. The LBW group had liver-specific insulin resistance associated with increased levels of PEPCK expression. These changes were associated with pituitary hyperplasia of the ACTH-secreting cells, increased morning plasma ACTH concentrations, elevated corticosterone secretion during restraint stress, and an ∼70% increase in 24-h urine corticosterone excretion. These data support the hypothesis that prenatal stress can result in chronic hyperactivity of the hypothalamic-pituitary-adrenal axis, resulting in increased plasma corticosterone concentrations, upregulation of hepatic gluconeogenesis, and hepatic insulin resistance.


Endocrines ◽  
2021 ◽  
Vol 2 (3) ◽  
pp. 334-347
Author(s):  
Laura Gianotti ◽  
Sara Belcastro ◽  
Salvatore D’Agnano ◽  
Francesco Tassone

The hypothalamic–pituitary–adrenal axis is a tightly regulated system that represents one of the body’s mechanisms for responding to acute and chronic stress. Prolonged stress and/or inadequate regulation of the stress system can lead to a condition of chronic hypercortisolism or, in some cases, a blunted cortisol response to stress, contributing to insulin resistance, increased adiposity and type 2 diabetes mellitus. Moreover, acute and chronic stress can exacerbate or worsen metabolic conditions by supporting an inflammatory state and a tight relationship between stress, inflammation and adipose tissue has been reported and has been a growing subject of interest in recent years. We reviewed and summarized the evidence supporting hypothalamic–pituitary–adrenal axis dysregulation as an important biological link between stress, obesity, inflammation and type 2 diabetes mellitus. Furthermore, we emphasized the possible role of infectious-related stress such as SarsCov2 infection in adrenal axis dysregulation, insulin resistance and diabetes in a bidirectional link. Understanding and better defining the links between stress and obesity or diabetes could contribute to further definition of the pathogenesis and the management of stress-related complications, in which the HPA axis dysregulation has a primary role.


2010 ◽  
Vol 222 (1) ◽  
pp. 125-134 ◽  
Author(s):  
Juan Beauquis ◽  
Françoise Homo-Delarche ◽  
Marie-Hélène Giroix ◽  
Jan Ehses ◽  
Josiane Coulaud ◽  
...  

2014 ◽  
Vol 60 (1) ◽  
pp. 84-92 ◽  
Author(s):  
Sílvia Paredes ◽  
Laura Ribeiro

Objective This article reviews the state of the art regarding the association between glucocorticoid actions and both obesity and insulin resistance, two main features of the metabolic syndrome. Methods A methodological assessment of the literature on PubMed and SciELO databases was conducted by using the following terms: stress, metabolic syndrome, glucocorticoids, obesity, insulin resistance, hypothalamic-pituitary-adrenal-axis and 11β-hydroxysteroid dehydrogenase. Results Chronic stress, mainly through hypothalamic-pituitary-adrenal axis dysregulation, promotes the accumulation of visceral fat. Reciprocally, obesity promotes a systemic low-grade inflammation state, mediated by increased adipokine secretion, which can chronically stimulate and disturb stress system. This vicious cycle, probably initiated by visceral adipose tissue dysfunction, might be the trigger for the development of metabolic syndrome. Conclusion Given the strong evidences linking glucocorticoid release, obesity and type 2 diabetes, better understanding of the mechanisms underlying this connection might be useful for prevention and treatment of the metabolic syndrome.


2015 ◽  
Vol 226 (2-3) ◽  
pp. 494-498 ◽  
Author(s):  
Katsutoshi Yokoyama ◽  
Takeshi Yamada ◽  
Hideaki Mitani ◽  
Sayaka Yamada ◽  
Shenghong Pu ◽  
...  

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