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Comment by Janice Cori Cobb on January 6, 2010 at 4:22am

Thank you for your prompt response to my query and for having called my attention to the Trier Social Stress Test of which I had previously been unaware.

Although it is cliche to comment on the inverse relationship between stress level and sleep loss, apropos of the deleterious effects of weight gain, you may find the forwarded abstract below (concerning IGF) from Obesity of interest.


Integrative Physiology

Obesity (2008) 16 7, 1516–1521. doi:10.1038/oby.2008.249

Polysomnographic Sleep, Growth Hormone Insulin-like Growth Factor-I Axis, Leptin, and Weight Loss

Michael H. Rasmussen1, Gordon Wildschiødtz2, Anders Juul3 and Jannik Hilsted1

1Department of Endocrinology, Hvidovre Hospital, University of Copenhagen, Hvidovre, Denmark
2Department of Psychiatry, University of Copenhagen, Copenhagen, Denmark
3Department of Growth and Reproduction, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
Correspondence: Michael H. Rasmussen (mhr@dadlnet.dk)

Received 24 October 2007; Accepted 2 March 2008; Published online 8 May 2008.

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Abstract
Short sleep appears to be strongly associated with obesity and altered metabolic function, and sleep and growth hormone (GH) secretion seems interlinked. In obesity, both the GH-insulin-like-growth-factor-I (GH-IGF-I) axis and sleep have been reported to be abnormal, however, no studies have investigated sleep in relation to the GH-IGF-I axis and weight loss in obese subjects. In this study polygraphic sleep recordings, 24-h GH release, 24-h leptin levels, free-IGF-I, total-IGF-I, IGF-binding protein-3 (IGFBP-3), acid-labile subunit (ALS), cortisol and insulin sensitivity were determined in six severely obese subjects (BMI: 41 1 kg/m2, 32 2 years of age), cross-sectional at baseline, and longitudinal after a dramatically diet-induced weight loss (36 7 kg). Ten age- and gender-matched nonobese subjects served as controls. Sleep duration (360 17 vs. 448 15 min/night; P < 0.01), 24-h GH (55 9 vs. 344 55 mU/l24 h; P < 0.01), free-IGF-I (2.3 0.42 vs. 5.7 1.2 g/l; P < 0.01), and total-IGF-I (186 21 vs. 301 18 g/l; P < 0.01) were significantly decreased and 24-h leptin levels were increased (35 5 vs. 12 3 g/l; P < 0.01) in obese subjects at pre-weight loss compared with nonobese subjects After diet-induced weight loss the differences in GH, free IGF-I, and leptin were no longer present between previously obese and nonobese subjects, whereas a significant difference in sleep duration and total IGF-I levels persisted. Rapid eye movement (REM) sleep, non-REM sleep, IGFBP-3, ALS, and cortisol levels were similar in obese and nonobese subjects. Sleep duration, 24-h GH, and IGF-I levels were decreased and 24-h leptin levels were increased in obese subjects. We conclude that hyposomatotropism and hyperleptinemia in obesity are transient phenomena reversible with weight loss, whereas short sleep seems to persist after weight has been reduced dramatically.

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Comment by Mario Belledonne on January 4, 2010 at 3:32am

Social stress associated changes in body fat have been found associated in monkeys. I do not know if somebody was able to do studies is humans or in minorities. There is interest on assessing the levels on cortisol and ACTH responses to psychosocial stress (Trier Social Stress Test) and pharmacological stimulation (1 microg ACTH(1-24), 0.5 mg dexamethasone). The point that I wanted to make was that renal responses to stress are unlikely to decrease blood flow to the kidneys to be have a direct pathogenic on the kidneys or to decrease GFR, independent of the effects of stress on hypertension, metabolic syndrome, diabetes, etc. and that determinations of sympathetic activity and cortisol levels will not tells us anything about renal function. Another important issue is whether responses to Trier Social Stress Test and the dexamethasone stimulation test has been validated in renal insufficiency.

Comment by Janice Cori Cobb on January 3, 2010 at 11:57pm

As an educator, I have noted chronic sympathetic activation particularly among students from minority groups.

During the 1980s the medical profession employed the "dexamethazone suppression test" in hopes to differentiate depression of an endogenous etiology from that which was "situational", and of, therefore deemed of lesser physiological consequence. Although subsequent investigations had revealed that any stressor(as perception of stress is entirely subjective) -- irrespective of etiology -- sufficient to induce chronic sympathetic activation -- will, in turn, induce chronic cortisol production.

Might then the dexamethazone suppression test be reintroduced in minority populations in order to screen for persons besieged by stress and, therefore, especially vulnerable to physiological (read renal) damage?

Comment by Janice Cori Cobb on January 3, 2010 at 11:44pm

You had once commented on the need to find a means that exceeds creatinine level through which to assess kidney dysfunction. To this end, the seminal investigations of Hans Seyle regarding human physiological adaptations to stress (G.A.S.S., "General Adaptation to Stress Syndrome") emphasized the deleterious sequellae associated with chronic sympathetic activation. Excessive stress-induced cortisol production -- as I have read in clinical journals and actually witnessed among non-diabetic students -- can induce, albeit temporarily, glycosuria. and ketonuria

Comment by Mario Belledonne on December 30, 2009 at 11:12pm

Catherine, I am very glad that you have no kidney dysfunction and that your healthy lifestyle could be the best medicine to prevent progression of kidney disease considering the risk factors you have. Also, it is important to monitor for urinary tract infection, hypertension, hyperlipidemia as well as detecting whether you have pre-diabetes – an abnormal glucose tolerance test (GTT). Pre-diabetes could be considered treated when the GTT becomes normal. There are studies that showed that we need to lose only 7% body weight with diet and exercise to prevent pre-diabetes to become diabetes. The objective of our group DPKC is to promote healthy diet and exercise as the first step in the prevention of diabetes, metabolic syndrome and cardio-renal disease. We need not only to raise awareness about these issues but we need to utilize tools such as social marketing as a way to change destructible behavior promoted by corporate interest.

Comment by Catherine Landerholm on December 30, 2009 at 7:53pm

I had gestational diabetes 16 years ago but I show no signs of it now. I was quite overweight at that time. Although I have been diagnosed with PKD I am showing no signs to date that would interrupt my active lifestyle.
I am however aware now, and knowledge is power. I am leaning to, although a novice and not a medical professional, the idea that what we eat/take into our bodies is directly affecting disease and progression of dormant genes that cause these diseases. Although I am 50 and very much used to the S.A.D. I am trying to learn and incorporate a Vegitarian Lifestyle, with much more antioxidants, soy and water into my diet. 2010 is a good time to start. I'll keep you all posted, lol. One day at a time.

Comment by Mario Belledonne on December 25, 2009 at 11:18pm

Thank you Janice for your enlighten comments. We all agree that there are genetic and environmental factors in play, and there are hypothesis to explain how certain populations have a higher incidence of metabolic syndrome, obesity and diabetes as compared to others. In most cases moderate weight loss attained by adequate diet and exercise or Metformin and/or has been shown to prevent or to control diabetes. http://diabetes.niddk.nih.gov/dm/pubs/preventionprogram/
The effort to prevent progression of diabetes into kidney failure and heart disease has only meet partial success. Despite hyperglycemia control, blood pressure control, hyperlipidemia treatments, and the "renal protective" treatments with angiotensin converting enzymes and receptor blockers, which have not reached goals, thus the incidence of end stage renal disease due to diabetes continues to rise. Diabetes is the leading cause of kidney failure, accounting for 44% of new cases in 2005. In 2005, 46,739 people with diabetes began treatment for end-stage kidney disease in the United States and Puerto Rico.
There is a need to increase awareness among the public and health providers about this problem. We need chronic disease management programs and more research to develop markers to detect which subjects will respond to specific type of treatments. Personally, I am working on the Renin Angiotensin Aldosterone system and how some individuals show abnormalities long before they have signs of diabetic nephropathy.

Best regards,

Mario Belledonne

Comment by Janice Cori Cobb on December 25, 2009 at 7:13am

Merry Christmas, Mario, thank you for your warm welcome.
As a student of molecular anthropology, I am intrigued by the existance of so-called "thrifty" genes that predominate certain Native American groups (e.g. the Pima), and effect, also, many Hispanic peoples as well.
This genetic make up, selected when our species was in it's infancy, and famines, frequent, confered to it's possesors a "reproductive advantage" -- those capable of retaining fat stores longer survived, whereas those incapable perished. In a world dominated by "junk food" and inactivity, populations typified by this genetic make-up, now face extinction from an especially treacherous triad -- hypertension, hyperlipidimia and hyperglycemia -- the "metabolic syndrome"!

We, as educators, must offer those within our reapective spheres of influence -- viable options to the ubiquitous fast foods that tempt unsuspecting minds and metabolisms by their notorious easy accessibility; their appeal sweetened by high fructose corn syrup, the devil in food.

Although we may initially appear to tread precariously on cherished beliefs
and traditions -- among many northern Alaskan peoples, a fat wife is considered the sign of a good hunter -- education sufficient such that good dietary choices are consistently made -- will claim genetically predisposed
populations for sound health before necessity sends them seeking treatment.

Regards,
Janice Cori Cobb
many cultures