Amerikanische Genforscher sorgten kurzfristig für nobelpreisverdächtige Aufmerksamkeit, indem sie fetten/trägen Mäusen Leptin spritzten und diese mal eben kurzfristig 30% Körpergewicht abwarfen. Das ging bei den Menschen aber voll in die Hose.
...ist zwar richtig, aber dennoch wird noch immer davon ausgegangen, dass Leptin auch beim Menschen eine entscheidende Rolle spielt (nur scheint die Sache hier etwas komplexer zu sein).
Z.B. führen Defekte (durch Mutationen) am Leptinrezeptor auch beim Menschen zu Übergewicht und der Ausgleich eines krankhaften Leptindefizites führt auch beim Menschen zur Gewichtsabnahme (sowie zur Erhöhung des Spiegels an Schilddrüsenhormonen).
Farooqi et al. schreiben z.B. im abstract ihres Artikels von 2001:
The adipocyte-derived hormone leptin is crucial for energy homeostasis in mammals; mice and humans without it suffer from a voracious appetite and extreme obesity. The effect on energy balance of variations in plasma leptin above a minimal threshold is uncertain, however, particularly in humans. Here we examine a group of individuals who are genetically partially deficient in leptin, and show that differences in circulating leptin levels within the range found in normal human populations can directly influence the laying down of fat tissue (adiposity).
Eine weitere Studie konnte zeigen, dass die Verabreichung von Leptin während einer Reduktionsdiät auch beim Menschen den Appetit verringerte.
Eine Verabreichung von Leptin beim diät-induzierten (Fasten) "Leptinmangel" hat auch beim Menschen sichtbare Auswirkungen:
Rosenbaum et al. 2002:
Maintenance of a reduced body weight is associated with decreased 24-hour energy expenditure, and decreased circulating concentrations of leptin and thyroid hormones. To determine whether these adaptive metabolic and endocrine changes are partly leptin-mediated, we measured body composition, aspects of energy expenditure, and circulating concentrations of leptin and thyroid hormones in 4 subjects at 3 time points: 1.) Usual body weight; 2.) While stable at 10% reduced body weight; and 3.) During a 5-week period at 10% reduced body weight while receiving twice per day leptin injections that restored 8 AM circulating leptin concentrations to those seen at usual body weight. During maintenance of a 10% reduced body weight, circulating T3, T4, and leptin concentrations were decreased. All of these endocrine changes were reversed by administration of "replacement" doses of leptin (r-metHuLeptin). Indirect calorimetry, and subtle changes in body composition associated with leptin administration, were used to calculate the net change in stored calories and in 24-hour energy expenditure. Total energy expenditure increased in all subjects during r-metHuLeptin administration. These data indicate that decrease leptin concentrations resulting from loss of fat mass account for some aspects of the endocrine/metabolic phenotype associated with the weight-reduced state.
Oder auch hier...
Chan et al. 2003:
To elucidate the role of leptin in regulating neuroendocrine and metabolic function during an acute fast, six to eight healthy, lean men were studied under four separate conditions: a baseline fed state and three 72-hour fasting studies with administration of either placebo, low-dose recombinant-methionyl human leptin (r-metHuLeptin), or replacement-dose r-metHuLeptin designed to maintain serum leptin at levels similar to those in the fed state. Replacement-dose r-metHuLeptin administered during fasting prevents the starvation-induced changes in the hypothalamic-pituitary-gonadal axis and, in part, the hypothalamic-pituitary-thyroid axis and IGF-1 binding capacity in serum. Thus, in normal men, the fall in leptin with fasting may be both necessary and sufficient for the physiologic adaptations of these axes, which require leptin levels above a certain threshold for activation. In contrast to findings in mice, fasting-induced changes in the hypothalamic-pituitary-adrenal, renin-aldosterone, and growth hormone-IGF-1 axes as well as fuel utilization may be independent of leptin in humans. The role of leptin in normalizing several starvation-induced neuroendocrine changes may have important implications for the pathophysiology and treatment of eating disorders and obesity.