Leptin receptors are highly expressed in areas of the hypothalamus known to be important in regulating body weight, as well as in T lymphocytes and vascular endothelial cells (See Practical Applications in www.semeioticabiofisica.it).
Such as physiological events represent the rationale of biophysical-semeiotic bedside evaluation of leptin concentrations, augmented in metabolic syndrome and often in advanced stages of pre-metabolic syndrome, classic and variant. Thus, the possibility of recognizing, for the first time clinically, leptin increase constitutes a diagnostic tool of essential importance, applicable on very large scale.
Recent studies with obese and non-obese humans demonstrated a strong positive correlation of serum leptin concentrations with percentage of body fat, and also that there was a higher concentration of ob mRNA in fat from obese compared to thin subjects. Genetically obese mices with inactivating mutations in the ob gene or the gene encoding the leptin receptor (db gene) have been known for many years and were instrumental in the initial cloning of the ob gene 2, 5, 6).
It appears that as adipocytes increase in size due to accumulation of triglyceride, they synthesize more and more leptin. In essence, leptin provides the body with an index of nutritional status. Leptin's effects on body weight are mediated through effects on hypothalamic centers that control feeding behavior and hunger, body temperature and energy expenditure.
Decreased hunger and food consumption, mediated at least in part by inhibition of neuropeptide Y synthesis. Neuropeptide Y is a very potent stimulator of feeding behavior.
Increased energy expenditure, measured as increased oxygen consumption, higher body temperature and loss of adipose tissue mass.
The mechanisms by which leptin exerts its effects on metabolism are largely unknown and are likely quite complex. In contrast to dieting, which results in loss of both fat and lean mass, treatment with leptin promotes lipolysis in adipose tissue, but has no apparent effect on lean tissue.
Recent studies in obese and non-obese humans demonstrated positive correlation between serum leptin concetration and percentage of body adipose tissue and highest presence of ob-m-RNA in adipose tissue than that observed in lean individuals (7). These data were corroborated clinically by Biophysycal Semeiotics (8).
Bibliografia.
1) Cherhab FF, Mounzih K, Lu R, Lim ME: Early onset of reproductive function in normal female mice treated with leptin. Science 275:88, 1997.
2) Clement K, Vaisse C, Lahlou N, et al: A mutation in the human leptin receptor gene causes obesity and pituitary dysfunction. Nature 392:398, 1998.
3) Considine RV, Sinha MK, Heiman ML etc: Serum immunoreactive-leptin concentrations in normal-weight and obese humans. New Eng J Med 334:292, 1996.
4) Friedman JM, Halaas JL: Leptin and the regulation of body weight in mammals. Nature 395:763, 1998.
5) Halaas JL, Gajiwala KS, Maffel M, etc: Weight-reducing effects of the plasma protein encoded by the obese gene. Science 269:543, 1995.
6) Montague CT, Faroozi IS, Whitehead JP, etc: Congenital leptin deficiency is associated with severe early-onset obesity in humans. Nature 387:903, 1997.
7) Pelleymounter MA, Cullen MJ, Baker MB, etc: Effects of the obese gene product on body weight regulation in ob/ob mice. Science 269:540, 1995.
8) Stagnaro S. Pre-metabolic syndrome: the real initial stage of metabolic-syndrome, type 2 diabetes and arteroscleropathy. Cardiovascular Diabetology 2004, 3:1
Cardiovascular Diabetology
Biophysical-Semeiotic Bedside Evaluation of Leptin.
29 November 2007
Sirs,
Leptin receptors are highly expressed in areas of the hypothalamus known to be important in regulating body weight, as well as in T lymphocytes and vascular endothelial cells (See Practical Applications in www.semeioticabiofisica.it).
Such as physiological events represent the rationale of biophysical-semeiotic bedside evaluation of leptin concentrations, augmented in metabolic syndrome and often in advanced stages of pre-metabolic syndrome, classic and variant. Thus, the possibility of recognizing, for the first time clinically, leptin increase constitutes a diagnostic tool of essential importance, applicable on very large scale.
Recent studies with obese and non-obese humans demonstrated a strong positive correlation of serum leptin concentrations with percentage of body fat, and also that there was a higher concentration of ob mRNA in fat from obese compared to thin subjects. Genetically obese mices with inactivating mutations in the ob gene or the gene encoding the leptin receptor (db gene) have been known for many years and were instrumental in the initial cloning of the ob gene 2, 5, 6).
It appears that as adipocytes increase in size due to accumulation of triglyceride, they synthesize more and more leptin. In essence, leptin provides the body with an index of nutritional status. Leptin's effects on body weight are mediated through effects on hypothalamic centers that control feeding behavior and hunger, body temperature and energy expenditure.
Decreased hunger and food consumption, mediated at least in part by inhibition of neuropeptide Y synthesis. Neuropeptide Y is a very potent stimulator of feeding behavior.
Increased energy expenditure, measured as increased oxygen consumption, higher body temperature and loss of adipose tissue mass.
The mechanisms by which leptin exerts its effects on metabolism are largely unknown and are likely quite complex. In contrast to dieting, which results in loss of both fat and lean mass, treatment with leptin promotes lipolysis in adipose tissue, but has no apparent effect on lean tissue.
Recent studies in obese and non-obese humans demonstrated positive correlation between serum leptin concetration and percentage of body adipose tissue and highest presence of ob-m-RNA in adipose tissue than that observed in lean individuals (7). These data were corroborated clinically by Biophysycal Semeiotics (8).
Bibliografia.
1) Cherhab FF, Mounzih K, Lu R, Lim ME: Early onset of reproductive function in normal female mice treated with leptin. Science 275:88, 1997.
2) Clement K, Vaisse C, Lahlou N, et al: A mutation in the human leptin receptor gene causes obesity and pituitary dysfunction. Nature 392:398, 1998.
3) Considine RV, Sinha MK, Heiman ML etc: Serum immunoreactive-leptin concentrations in normal-weight and obese humans. New Eng J Med 334:292, 1996.
4) Friedman JM, Halaas JL: Leptin and the regulation of body weight in mammals. Nature 395:763, 1998.
5) Halaas JL, Gajiwala KS, Maffel M, etc: Weight-reducing effects of the plasma protein encoded by the obese gene. Science 269:543, 1995.
6) Montague CT, Faroozi IS, Whitehead JP, etc: Congenital leptin deficiency is associated with severe early-onset obesity in humans. Nature 387:903, 1997.
7) Pelleymounter MA, Cullen MJ, Baker MB, etc: Effects of the obese gene product on body weight regulation in ob/ob mice. Science 269:540, 1995.
8) Stagnaro S. Pre-metabolic syndrome: the real initial stage of metabolic-syndrome, type 2 diabetes and arteroscleropathy. Cardiovascular Diabetology 2004, 3:1
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Competing interests
None declared