Stick it in your rear - OLD MAN WINTER!!!
That's right old man winter, I'm talking to YOU! You can blow right back to where you blew in from! I'm tired of stretching out my shoes because I have to wear 3 pairs of socks. I am tired of looking like I gained 15 lbs overnight because I have 3 layers of clothes on and more than anything else..........
I am tired of freezing and shivering no matter how many layers I have on!
So stick it in your rear Old Man Winter. I no longer claim you! You may leave now and stay away for the next ohhhhhhh 3 or 4 years.
Sincerely,
Gigee
This is from an article in 2004 about Leptin and obesity. What interests me personally was this part...
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The research team found that leptin triggers production of the active form of a peptide - áMSH - in the hypothalamus, the small area in the base of the brain that controls hunger and metabolism. Researchers say this peptide, or small protein, is one of the body's most powerful metabolism booster signals, sending a fast, strong message to the brain to burn calories.
This message is then sent to another part of the hypothalamus, where another peptide is produced and released. This stimulates the pituitary gland, which secretes a hormone that relays the message to the thyroid, the master of metabolism. Once activated, the thyroid gland then spreads word to the body's cells to increase energy production.
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My PCP once said to me that between my thyroid and PCOS that my metabolism is screwed (her word, not mine). Now, RNY didn't cure my thyroid or my PCOS so I still have the metabolism problems.
So I have to be careful and if Leptin has something to do with it then I do want to know all I can about it. I do not ever want to go back from whence I came!!
So I am beginning to research it more, I can see that you are. We'll have to share our information one day and see if we come up with the same stuff.
Hey!!?? I guess we could look at shivering as a form of excercise? *grin*
Gigee
Check this out Rob. From a study done in 2004:
Phenotypic effects of leptin replacement on morbid obesity, diabetes mellitus, hypogonadism, and behavior in leptin-deficient adults
Julio Licinio * , Sinan Caglayan * ¶, Metin Ozata ¶, Bulent O. Yildiz *, Patricia B. de Miranda , Fiona O'Kirwan *, Robert Whitby *, Liyin Liang *, Pinchas Cohen ||, Shalender Bhasin **, Ronald M. Krauss , Johannes D. Veldhuis , Anthony J. Wagner , Alex M. DePaoli , Samuel M. McCann ¶¶, and Ma-Li Wong *
*Center for Pharmacogenomics, Neuropsychiatric Institute, Department of Psychiatry and Biobehavioral Sciences, Department of Medicine, Division of Endocrinology, Diabetes, and Hypertension, General Clinical Research Center, and ||Department of Pediatrics, Division of Pediatric Endocrinology, David Geffen School of Medicine, University of California, Los Angeles, CA 90095-1761; ¶Department of Endocrinology and Metabolism, Gulhane Haydarpasa Training Hospital, Acibadem-Istanbul 34660, Turkey; **Division of Endocrinology, Department of Internal Medicine, Charles R. Drew University of Medicine and Science, University of California, Los Angeles, CA 90059; Children's Hospital Oakland Research Institute, University of California at Berkeley, Oakland, CA 94609; Division of Endocrinology and Metabolism, Department of Internal Medicine, Mayo Medical and Graduate School of Medicine, Mayo Clinic, Rochester, MN 55905; Department of Clinical Research, Amgen Inc., Thousand Oaks, CA 91320; and ¶¶Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, LA 70808-4124
Contributed by Samuel M. McCann, December 31, 2003
Genetic mutations in the leptin pathway can be a cause of human obesity. It is still unknown whether leptin can be effective in the treatment of fully established morbid obesity and its endocrine and metabolic consequences in adults. To test the hypothesis that leptin has a key role in metabolic and endocrine regulation in adults, we examined the effects of human leptin replacement in the only three adults identified to date who have genetically based leptin deficiency. We treated these three morbidly obese **** ygous leptin-deficient adult patients with recombinant human leptin at low, physiological replacement doses in the range of 0.01-0.04 mg/kg for 18 months.
Patients were hypogonadal, and one of them also had type 2 diabetes mellitus.
We chose the doses of recombinant methionyl human leptin that would achieve normal leptin concentrations and administered them daily in the evening to model the normal circadian variation in endogenous leptin.
The mean body mass index dropped from 51.2 ± 2.5 (mean ± SEM) at baseline to 26.9 ± 2.1 kg/m2 after 18 months of treatment, mainly because of loss of fat mass.
We document here that leptin replacement therapy in leptin-deficient adults with established morbid obesity results in profound weight loss, increased physical activity, changes in endocrine function and metabolism, including resolution of type 2 diabetes mellitus and hypogonadism, and beneficial effects on ingestive and noningestive behavior.
These results highlight the role of the leptin pathway in adults with key effects on the regulation of body weight, gonadal function, and behavior.
Diane!
The research is becoming fascinating. Especially when you find things that show a study done on obese patients where they use Leptin replacement and the study resulted in what they termed profound weight loss as well as many other good things. Now this study was done in 2004.
I have to research more to see if they ended finding negative results after a point and time or if the FDA just hasn't approved this type of treatment for obesity.
Fun huh?
Gigee