Neuroendocrine mechanisms in insulin resistance

Abstract

Dysregulated hormonal, metabolic and neural signalling within and between organs can contribute to development of metabolic diseases including type 2 diabetes. Insulinantagonistic effects of hormones, cytokines and excess metabolic substrates such as glucose and fatty acids may be exerted via common mechanisms involving for example reactive oxygen species (ROS) accumulation and associated inflammatory responses.Visceral adiposity is a central component of the metabolic syndrome and it is also strongly associated with insulin resistance. Both visceral obesity and insulin resistance are important risk factors for the development of type 2 diabetes. In the development of insulin resistance, it is likely that intra-abdominal adipose tissue plays a critical role in a complex endocrine and neural network involving several tissues. This review paper focuses on neuroendocrine 'stress' factors that target insulin-responsive tissues, in particular adipose tissue. We propose that there are common pathways by which dysregulation in different endocrine systems may contribute to the development of type 2 diabetes.

Effects of Noise Exposure on Systemic and Tissue-Level Markers of Glucose Homeostasis and Insulin Resistance in Male Mice

“…These findings should also be confirmed in female mice. Factors that may contribute to insulin resistance at the tissue level (e.g., inflammatory mediators, such as cytokines and chemokines, and reactive oxygen species, such as superoxide or hydroxyl radicals) (Sjöstrand and Eriksson 2009; Tiganis 2011), should also be investigated (through immunoblots, immunohistochemical methods, and quantitative polymerase chain reaction) to pinpoint the exact mechanisms of the diabetogenic effects of noise exposure.…”

“…Persistently elevated cortisol levels have been proposed to result in insulin resistance and are associated with the development of T2DM (Sjöstrand and Eriksson 2009). For example, subjects with a syndrome of cortisol excess (Cushing syndrome) showed increased insulin resistance (Nosadini et al 1983).…”

The immunosuppressive agents rapamycin, cyclosporin A and tacrolimus increase lipolysis, inhibit lipid storage and alter expression of genes involved in lipid metabolism in human adipose tissue

“…sympathetic and parasympathetic, control of adipose tissue metabolism (Kreier et al, 2002;Sjostrand and Eriksson, 2009). Thus, the findings in this study should be confirmed with in vivo experiments.…”

Molecular Basis of Insulin Resistance and Its Relation to Metabolic Syndrome

“…In addition, many obese subjects do not have metabolic abnormalities. Systemic chronic inflammation [39] , on the other hand, paints the most complete picture of insulin resistance as it is the result of all altered cytokine production and signaling pathways in the body. A more accessible marker for this inflammation can be obtained by measuring C-reactive protein (CRP); 40% of our patients with MetS had an elevated CRP.…”