dysregulated cortisol metabolism plays a role in obesity. This study looked at obese men. Decreased liver 11-betaHSD1 activity was found in the liver, with decreased cortisone to cortisol conversion. Additionally, increase cortisol metabolites were found. However, there was found to be an increase in 11-betaHSD1 activity in the adipose tissue increasing the cortisone to cortisol conversion indicating an increase in peripheral cortisol production.
increased 11-betaHSD type 1 and increased 5-alpha reductase activity found to be associated with generalized obesity in men. Both indicate increased cortisone to cortisol production.
Increased visceral adiposity results in increased 11beta-HSD that results in increased cortisone to cortisol production preference. Cortisol production doesn't just come from the adrenals--it is also produced and metabolized in peripheral and visceral fat.
Abstract only available. Cortisol-cortisone shuttle play a role in hypertension. Those with 11betaHSD type II defects will have elevated blood pressure due to increase in mineralcorticoids.
Areas of high exposure of Dioxin in Vietnam found to have associated elevated salivary cortisol, cortisone, and DHEA. Now, this can only be seen as an association, but they did find these elevations only in the "hot spots" and not in low exposure areas.
obesity is associated with increased cortisol metabolism. This would be found in increased urinary metabolites, especially via the 5-allpha reductase pathway. Increased cortisone to cortisol production occurs via 11 beta-HSD1. This occurs predominately in adipose tissue. The thought here is cortisol metabolism is tissue specific and functionally different.
LC-MS/MS shown to be reliable in salivary cortisol evaluation. Obese individuals create special challenges with regards to coritsol levels, due to peripheral cortisol to cortisone conversion.
This study points out that saliva should not be used solely in the diagnosis of Cushing's syndrome due to unreferenced norms. That however, doesn't nullify salivary cortisol. It requires a look at the references. for those that are obese and being evaluated for cushing's. There is no perfect test. T
This study is a little misleading in its conclusion. Salivary testing is valid, but the reference ranges in the obese with suspected cushing's syndrome needs further evaluation: according to these authors.
adipocytes increase genetic expression of 11beta-HSD. This increases local cortisol production from cortisone. This plays a pivotal role in obesity. Question: would this play a role in peripheral hypothyroid? I think so.
GH deficiency effectively increases cortisol production in key target tissues including liver and adipose tissue, promoting insulin resistance and visceral adiposity
GH/IGF-I modulation of cortisol metabolism may underpin the pathogenesis of common diseases such as central obesity
Patients with central obesity but with no evidence of hypopituitarism have relative GH deficiency and it is exciting to speculate that low-dose GH treatment in this group, by inhibiting cortisol generation within omental fat, may offer a novel therapeutic approach.
GH plays a key regulating role in obesity. GH deficiency promotes increased cortisone to cortisol production in adipose tissue and liver. This promotes insulin resistance and obesity.
fat cells appear to have elevated expression of 11beta-hydroxysteriod dehydrogenase type I, which results in increased conversion of cortisol to cortisone.
This study reveals the degree of metabolism dysfunction in obesity. This study suggests that cortisol metabolism is increased in obesity, which results in increased HPA activity resulting in increased peripheral cortisol production. The question to be asked: is serum, salivary, and urinary cortisol results revealing the same function of cortisol. The answer is no.
acute GC secretion during stress mobilizes peripheral amino acids from muscle as well as fatty acids and glycerol
from peripheral fat stores to provide substrates for glucose synthesis by the liver
chronically elevated GC levels
alter body fat distribution and increase visceral adiposity as well as metabolic abnormalities in a fashion reminiscent of
metabolic syndrome
This local production may
play an important role in the onset of obesity and insulin resistance.
In adipocytes, cortisol inhibits lipid mobilization in the presence of insulin, thus leading to triglyceride accumulation
and retention.
Since the density of GC receptors is higher in intra-abdominal (visceral) fat than in other fat depots, the
activity of cortisol leading to accumulation of fat is accentuated in visceral adipose tissue (24, 158), providing a mechanism by which excessive endogenous or exogenous GC lead to abdominal obesity and IR
obese patients generally have normal or subnormal
plasma cortisol concentrations
This may be explained by an increased intratissular/cellular concentration of cortisol in adipose tissues
Intracellular GC may be produced from recycling of GC metabolites such as cortisone in adipose tissues
Local GC recycling metabolism is mediated by 11β-hydroxysteroid dehydrogenase enzymes (11β-HSD1 and 11β-HSD2
Cortisol also increases 11β-HSD1 expression in human adipocytes
In humans, elevated 11β-HSD1 expression in visceral adipose tissue is also associated with obesity
even if obese patients generally have normal or subnormal plasma cortisol concentrations
(131, 158), triglyceride accumulation in visceral adipose tissue may be due, at least in part, to the local production of GC in insulin-
and GC-responsive organs such as adipose tissue, liver, and skeletal muscle
Alterations in the HPA and hypothalamic-pituitary-gonadal axes with a resultant decrease in testosterone:cortisol ratios have been implicated in OTS. Proinflammatory cytokines are potent activators of the HPA system, which cause release of corticotropin-releasing hormone, adrenocorticotropic hormone, and cortisol. These cytokines suppress testosterone through central inhibition
Some have suggested that a decreased testosterone:cortisol ratio can be diagnostic of NFO and/or OTS. However, the ratio represents the physiologic strain of training rather than the athlete’s maladaption to that stress
Cortisol (catabolic and anti-inflammatory) is converted to inactive cortisone by 11β-HSD2
A prospective study found a clinically significant increase in overnight urinary cortisol:cortisone ratio during a high training load period in triathletes, who subsequently underperformed and reported fatigue
It is proposed that cytokines may inhibit 11β-HSD2 activity and result in relative increases in cortisol and, hence, catabolism