Big Bad Buff said:
OMG, are you for real? One of the functions of cortisol is to trigger a glucocorticoid effect - helping the body produce blood sugar from proteins. Excess glucose is then used for lipogenesis (fat production).
For someone that claims to be so well read on the topic you lack even the most basic understanding of cortisol.
I don't know what to say bro...so the body breaks down protein in order to store more fat? I don't think so. It breaks it down in order to use it as energy.
A few studies on normal humans:
Title: Neuroendocrine perturbations as a cause of insulin resistance.
Author, Editor, Inventor: Bjorntorp-Per {a}
Author Address: {a} Department of Heart and Lung Diseases, Sahlgren's Hospital, University of Goteborg, S-413 45, Goteborg, Sweden
Source: Diabetes-Metabolism-Research-and-Reviews. Nov.-Dec., 1999; 15 (6): 427-441.
Publication Year: 1999
Document Type: Article-
ISSN (International Standard Serial Number): 1520-7552
Language: English
Language of Summary: English
Abstract: Insulin resistance is followed by several prevalent diseases. The most common condition with insulin resistance is obesity, particularly when localized to abdominal, visceral regions. A summary of recent reviews on the pathogenesis of systemic insulin resistance indicates that major factors are decreased insulin effects on muscular glycogen synthase or preceding steps in the insulin signalling cascade, on endogenous glucose production and on circulating free fatty acids (FFA) from adipose tissue lipolysis. Contributions of morphologic changes in muscle and other factors are considered more uncertain. Newly developed methodology has made it possible to determine more precisely the neuroendocrine abnormalities in abdominal obesity including increased cortisol and adrenal androgen secretions. This is probably due to a hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis, amplified by inefficient feedback inhibition by central glucocorticoid receptors, associated with molecular genetic defects. Secondly, secretion of gender-specific sex steroid hormones becomes inhibited and the sympathetic nervous system activated. At this stage the HPA axis shows signs of a 'burned-out' condition, and cortisol secretion is no longer elevated.
Cortisol counteracts the insulin activation of glycogen synthase in muscle, the insulin inhibition of hepatic glucose production and the
insulin inhibition of lipolysis in adipose tissue, leading to the well-established systemic insulin resistance caused by excess cortisol. This is exaggerated by increased free fatty acid mobilization, particularly with a concomitant elevation of the activity of the sympathetic nervous system. Furthermore, capillarization and fiber composition in muscle are changed. These are the identical perturbations responsible for insulin resistance in recent reviews. The diminished sex steroid secretion in abdominal obesity has the same consequences. It is thus clear that insulin resistance may be induced by neuroendocrine abnormalities, such as those seen in abdominal obesity. These endocrine perturbations also direct excess fat to visceral fat depots via mechanisms that are largely known, indicating why abdominal obesity is commonly associated with insulin resistance. This possible background to the most prevalent condition of insulin resistance has been revealed by development of methodology that allows sufficiently sensitive measurements of HPA axis activity. These findings demonstrate the power of neuroendocrine regulations for somatic health.
Title: Effect of cortisol on energy expenditure and amino acid metabolism in humans.
Author, Editor, Inventor: Brillon-D-J; Zheng-B; Campbell-R-G; Matthews-D-E {a}
Author Address: {a} Cornell Univ. Med. Coll., 1300 York Ave., Box 149, New York, NY 10021, USA
Source: American-Journal-of-Physiology. 1995; 268 (3 PART 1) E501-E513.
Publication Year: 1995
Document Type: Article-
ISSN (International Standard Serial Number): 0002-9513
Language: English
Abstract: Hydrocortisone was infused overnight into nine normal healthy adults on three occasions at 0, 80, and 200 mu-g.kg-1.h-1, producing plasma cortisol concentrations of 10.6 +- 1.2, 34.0 +- 2.0, and 64.9 +- 4.3 mu-g/dl, respectively. L-(1-13C)leucine, L-(phenyl-2H-5)phenylalanine, and L-(2-15N)glutamine were infused during the last 7 h of hypercortisolemia to measure amino acid kinetics. During the last 3.5 h, somatostatin, glucagon, and insulin were infused to reduce the cortisol-induced elevation in plasma insulin to basal.
Hypercortisolemia increased plasma glucose, free fatty acid (FFA), and insulin concentrations. Institution of the somatostatin clamp returned insulin to basal but increased glucose and FFA.
Acute hypercortisolemia increased protein breakdown 5-20%, as measured by increases in leucine and phenylalanine appearance rates. Normalizing insulin during hypercortisolemia did not alter phenylalanine flux but enhanced leucine appearance rate, the fatter result indicating that insulin was affecting leucine metabolism during hypercortisolemia. The fraction of the leucine flux that was oxidized was not significantly increased with hypercortisolemia, but disposal by the nonoxidative route of leucine uptake for protein synthesis was increased. Hypercortisolemia increased cycling of amino acids by increasing protein breakdown and synthesis, but the increase in this process could have increased resting energy expenditure (REE) only 1-2%. Hypercortisolemia increased glutamine flux in a dose-dependent fashion through an increase in de novo synthesis, which presumably reflects increased release from skeletal muscle. Hypercortisolemia increased REE 9-15% at the 80 and 200 mu-g cntdot kg-1 cntdot h-1 infusion rates.
Respiratory quotient did not rise with cortisol infusion but tended to decrease, suggesting that the increase in REE was fueled by increased oxidation of fat. These data demonstrate that hypercortisolemia increases metabolic rate and may be in part responsible for the hypermetabolic state in injury.
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