Skip to main content
Erschienen in: CardioVasc 3/2018

24.05.2018 | Adipositas | Fortbildung

Die Set-Point-Theorie

Warum ist dauerhaft abnehmen so schwer?

verfasst von: Özlem Özcan, Prof. Dr. med. Werner Kern

Erschienen in: CardioVasc | Ausgabe 3/2018

Einloggen, um Zugang zu erhalten

Zusammenfassung

Die Zahl der Adipösen nimmt weltweit stetig zu. Maßnahmen zur Gewichtsreduktion gibt es mehrere, doch keine der Therapien kann langfristig eine erneute Gewichtszunahme verhindern. Der Körper versucht durch metabolische, hormonelle und neurochemische Kompensationsmechanismen, die sich im Laufe der Evolution entwickelt haben, das über eine längere Zeit erreichte Höchstgewicht, den Set-Point, zu schützen.
Literatur
3.
Zurück zum Zitat World Health Organization. Obesity: Preventing and Managing the Global Epidemic. World Health Organization: Geneva, Switzerland, 1998. World Health Organization. Obesity: Preventing and Managing the Global Epidemic. World Health Organization: Geneva, Switzerland, 1998.
4.
Zurück zum Zitat Zhang Y, Proenca R, Maffei M et al. Positional cloning of the mouse obese gene and its human homologue. Nature. 1994;372(6505):425–32CrossRefPubMed Zhang Y, Proenca R, Maffei M et al. Positional cloning of the mouse obese gene and its human homologue. Nature. 1994;372(6505):425–32CrossRefPubMed
5.
Zurück zum Zitat Greenberg JA, Boozer CN. The leptin-fat ratio is constant, and leptin may be part of two feedback mechanisms for maintaining the body fat set point in non-obese male Fischer 344 rats. Horm Metab Res. 1999;31(9):525–32CrossRefPubMed Greenberg JA, Boozer CN. The leptin-fat ratio is constant, and leptin may be part of two feedback mechanisms for maintaining the body fat set point in non-obese male Fischer 344 rats. Horm Metab Res. 1999;31(9):525–32CrossRefPubMed
6.
Zurück zum Zitat Woods SC, Seeley RJ. Understanding the physiology of obesity: review of recent developments in obesity research. Int J Obes Relat Metab Disord. 2002;26 Suppl 4:S8–S10CrossRefPubMed Woods SC, Seeley RJ. Understanding the physiology of obesity: review of recent developments in obesity research. Int J Obes Relat Metab Disord. 2002;26 Suppl 4:S8–S10CrossRefPubMed
7.
Zurück zum Zitat Badman MK, Flier JS. The gut and energy balance: visceral allies in the obesity wars. Science. 2005;307(5717):1909–14CrossRefPubMed Badman MK, Flier JS. The gut and energy balance: visceral allies in the obesity wars. Science. 2005;307(5717):1909–14CrossRefPubMed
8.
Zurück zum Zitat Secher A, Jelsing J, Baquero AF et al. The arcuate nucleus mediates GLP-1 receptor agonist liraglutide-dependent weight loß. J Clin Invest. 2014;124(10):4473–88CrossRefPubMedPubMedCentral Secher A, Jelsing J, Baquero AF et al. The arcuate nucleus mediates GLP-1 receptor agonist liraglutide-dependent weight loß. J Clin Invest. 2014;124(10):4473–88CrossRefPubMedPubMedCentral
9.
Zurück zum Zitat Sumithran P, Prendergast LA, Delbridge E et al. Long-term persistence of hormonal adaptations to weight loß. N Engl J Med. 2011;365(17):1597–604CrossRefPubMed Sumithran P, Prendergast LA, Delbridge E et al. Long-term persistence of hormonal adaptations to weight loß. N Engl J Med. 2011;365(17):1597–604CrossRefPubMed
10.
Zurück zum Zitat Schwartz A, Doucet E. Relative changes in resting energy expenditure during weight loß: a systematic review. Obes Rev. 2010;11(7):531–47CrossRefPubMed Schwartz A, Doucet E. Relative changes in resting energy expenditure during weight loß: a systematic review. Obes Rev. 2010;11(7):531–47CrossRefPubMed
11.
Zurück zum Zitat Doucet E, Imbeault P, St-Pierre S et al. Appetite after weight loß by energy restriction and a low-fat diet-exercise follow-up. Int J Obes Relat Metab Disord. 2000;24(7):906–14CrossRefPubMed Doucet E, Imbeault P, St-Pierre S et al. Appetite after weight loß by energy restriction and a low-fat diet-exercise follow-up. Int J Obes Relat Metab Disord. 2000;24(7):906–14CrossRefPubMed
12.
Zurück zum Zitat De Jonghe BC, Hayes MR, Bence KK. Melanocortin control of energy balance: evidence from rodent models. Cellular and Molecular Life Sciences. 2011;68(15):2569–2588CrossRefPubMed De Jonghe BC, Hayes MR, Bence KK. Melanocortin control of energy balance: evidence from rodent models. Cellular and Molecular Life Sciences. 2011;68(15):2569–2588CrossRefPubMed
13.
Zurück zum Zitat Luchtman DW, Chee MJ, Doslikova B et al. Defense of Elevated Body Weight Setpoint in Diet-Induced Obese Rats on Low Energy Diet Is Mediated by Loß of Melanocortin Sensitivity in the Paraventricular Hypothalamic Nucleus. PLoS One. 2015;10(10):e0139462CrossRefPubMedPubMedCentral Luchtman DW, Chee MJ, Doslikova B et al. Defense of Elevated Body Weight Setpoint in Diet-Induced Obese Rats on Low Energy Diet Is Mediated by Loß of Melanocortin Sensitivity in the Paraventricular Hypothalamic Nucleus. PLoS One. 2015;10(10):e0139462CrossRefPubMedPubMedCentral
14.
Zurück zum Zitat Kern W. Therapie der Adipositas und physiologische Regelungsmechanismen. Adipositas. 2017;11(2):100–7 Kern W. Therapie der Adipositas und physiologische Regelungsmechanismen. Adipositas. 2017;11(2):100–7
15.
Zurück zum Zitat Chhabra KH, Adams JM, Jones GL et al. Reprogramming the body weight set point by a reciprocal interaction of hypothalamic leptin sensitivity and POMC gene expreßion reverts extreme obesity. Mol Metab. 2016;5(10):869–81CrossRefPubMedPubMedCentral Chhabra KH, Adams JM, Jones GL et al. Reprogramming the body weight set point by a reciprocal interaction of hypothalamic leptin sensitivity and POMC gene expreßion reverts extreme obesity. Mol Metab. 2016;5(10):869–81CrossRefPubMedPubMedCentral
16.
Zurück zum Zitat Kälin S, Heppner FL, Bechmann I et al. Hypothalamic innate immune reaction in obesity. Nat Rev Endocrinol. 2015;11(6):339–51CrossRefPubMed Kälin S, Heppner FL, Bechmann I et al. Hypothalamic innate immune reaction in obesity. Nat Rev Endocrinol. 2015;11(6):339–51CrossRefPubMed
17.
Zurück zum Zitat Bray GA, Frühbeck G, Ryan DH, Wilding JP. Management of obesity. Lancet. 2016;387(10031):1947–56CrossRefPubMed Bray GA, Frühbeck G, Ryan DH, Wilding JP. Management of obesity. Lancet. 2016;387(10031):1947–56CrossRefPubMed
19.
20.
Zurück zum Zitat Arita Y, Kihara S, Ouchi N et al. Paradoxical decrease of an adipose-specific protein, adiponectin, in obesity. Biochem Biophys Res Commun. 1999;257(1):79–83CrossRefPubMed Arita Y, Kihara S, Ouchi N et al. Paradoxical decrease of an adipose-specific protein, adiponectin, in obesity. Biochem Biophys Res Commun. 1999;257(1):79–83CrossRefPubMed
21.
Zurück zum Zitat Tilg H, Moschen AR. Role of adiponectin and PBEF/visfatin as regulators of inflammation: involvement in obesity-aßociated diseases. Clin Sci (Lond). 2008;114(4):275–88CrossRef Tilg H, Moschen AR. Role of adiponectin and PBEF/visfatin as regulators of inflammation: involvement in obesity-aßociated diseases. Clin Sci (Lond). 2008;114(4):275–88CrossRef
22.
23.
Zurück zum Zitat Batterham RL, Le Roux CW, Cohen MA et al. Pancreatic polypeptide reduces appetite and food intake in humans. J Clin Endocrinol Metab. 2003;88(8):3989–92CrossRefPubMed Batterham RL, Le Roux CW, Cohen MA et al. Pancreatic polypeptide reduces appetite and food intake in humans. J Clin Endocrinol Metab. 2003;88(8):3989–92CrossRefPubMed
24.
Zurück zum Zitat Clark A, Nilßon MR. Islet amyloid: a complication of islet dysfunction or an aetiological factor in Type 2 diabetes? Diabetologia. 2004;47(2):157–69CrossRefPubMed Clark A, Nilßon MR. Islet amyloid: a complication of islet dysfunction or an aetiological factor in Type 2 diabetes? Diabetologia. 2004;47(2):157–69CrossRefPubMed
25.
Zurück zum Zitat Drucker DJ, Nauck MA. The Incretin System: Glucagon-like Peptide-1 Receptor Agonists and Dipeptidyl peptidase-4 Inhibitors in Type 2 Diabetes. Lancet. 2006;368:1696–1705CrossRefPubMed Drucker DJ, Nauck MA. The Incretin System: Glucagon-like Peptide-1 Receptor Agonists and Dipeptidyl peptidase-4 Inhibitors in Type 2 Diabetes. Lancet. 2006;368:1696–1705CrossRefPubMed
26.
Zurück zum Zitat Gault VA, O’Harte FP, Flatt PR. Glucose-dependent insulinotropic polypeptide (GIP): anti-diabetic and anti-obesity potential? Neuropeptides. 2003;37(5):253–63CrossRefPubMed Gault VA, O’Harte FP, Flatt PR. Glucose-dependent insulinotropic polypeptide (GIP): anti-diabetic and anti-obesity potential? Neuropeptides. 2003;37(5):253–63CrossRefPubMed
27.
Zurück zum Zitat Sakata I, Nakamura K, Yamazaki M et al. Ghrelin-producing cells exist as two types of cells, closed- and opened-type cells, in the rat gastrointestinal tract. Peptides. 2002;23(3):531–6CrossRefPubMed Sakata I, Nakamura K, Yamazaki M et al. Ghrelin-producing cells exist as two types of cells, closed- and opened-type cells, in the rat gastrointestinal tract. Peptides. 2002;23(3):531–6CrossRefPubMed
28.
Zurück zum Zitat Wynne K, Stanley S, McGowan B, Bloom S. Appetite control. J Endocrinol. 2005;184(2):291–318CrossRefPubMed Wynne K, Stanley S, McGowan B, Bloom S. Appetite control. J Endocrinol. 2005;184(2):291–318CrossRefPubMed
29.
Zurück zum Zitat Chelikani PK, Haver AC, Reidelberger RD. Intravenous infusion of peptide YY(3-36) potently inhibits food intake in rats. Endocrinology. 2005;146(2):879–8CrossRefPubMed Chelikani PK, Haver AC, Reidelberger RD. Intravenous infusion of peptide YY(3-36) potently inhibits food intake in rats. Endocrinology. 2005;146(2):879–8CrossRefPubMed
30.
Zurück zum Zitat Mann T, Tomiyama AJ, Westling E et al. Medicare’s search for effective obesity treatments: diets are not the answer. Am Psychol. 2007;62(3):220–33CrossRefPubMed Mann T, Tomiyama AJ, Westling E et al. Medicare’s search for effective obesity treatments: diets are not the answer. Am Psychol. 2007;62(3):220–33CrossRefPubMed
31.
Zurück zum Zitat Wadden TA. Treatment of obesity by moderate and severe caloric restriction. Results of clinical research trials. Ann Intern Med. 1993;119(7 Pt 2):688–93CrossRefPubMed Wadden TA. Treatment of obesity by moderate and severe caloric restriction. Results of clinical research trials. Ann Intern Med. 1993;119(7 Pt 2):688–93CrossRefPubMed
Metadaten
Titel
Die Set-Point-Theorie
Warum ist dauerhaft abnehmen so schwer?
verfasst von
Özlem Özcan
Prof. Dr. med. Werner Kern
Publikationsdatum
24.05.2018
Verlag
Springer Medizin
Schlagwörter
Adipositas
Adipositas
Erschienen in
CardioVasc / Ausgabe 3/2018
Print ISSN: 1617-4933
Elektronische ISSN: 1618-3851
DOI
https://doi.org/10.1007/s15027-018-1366-3

Weitere Artikel der Ausgabe 3/2018

CardioVasc 3/2018 Zur Ausgabe

Update Kardiologie

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.