La alteración hipotalámica en la obesidad HORMONAS Y CIRCUITOS NEURONALES
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may 31, 2023
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https://doi.org/10.36677/medicinainvestigacion.v11i1.19791
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Haydée Torres Guerrero, Dra
http://orcid.org/0000-0003-1928-0826
Ricardo Jair Ramírez Carreto, QFB
http://orcid.org/0000-0002-8032-806X
Yesica María Rodríguez Cortés, M en C
http://orcid.org/0000-0002-7664-8642
Anahí Chavarría Krauser, Dra.
http://orcid.org/0000-0002-6412-0461
http://orcid.org/0000-0003-1928-0826
Ricardo Jair Ramírez Carreto, QFB
http://orcid.org/0000-0002-8032-806X
Yesica María Rodríguez Cortés, M en C
http://orcid.org/0000-0002-7664-8642
Anahí Chavarría Krauser, Dra.
http://orcid.org/0000-0002-6412-0461
Resumen
El hipotálamo es el centro de regulación neuroendocrina de la homeostasis energética y del apetito. El mal desarrollo o el daño a los núcleos hipotalámicos involucrados alteran el equilibrio entre ingesta y gasto de energía, lo que conduce a un rápido aumento de peso. Distintas poblaciones neuronales, particularmente del núcleo arqueado del hipotálamo, detectan el estado nutricional del organismo e integran señales de hormonas periféricas, incluidas la insulina producida en el páncreas y la leptina, derivada de los adipocitos para regular la ingesta de calorías, el metabolismo de la glucosa y el gasto de energía. En México los niveles de obesidad se han incrementado de forma alarmante en las últimas décadas y mundialmente se considera un problema de salud pública, por lo que, para dar solución a este problema se requiere de una mejor comprensión de las causas subyacentes del aumento de peso y sus comorbilidades metabólicas asociadas como la diabetes mellitus tipo 2, entre otras. Esta revisión se enfoca en la descripción general de la regulación dependiente de la homeostasis energética del sistema nervioso central ilustra cómo la desregulación de los circuitos neuronales involucrados puede conducir a la sobre nutrición y la obesidad.
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TORRES GUERRERO, Haydée et al.
La alteración hipotalámica en la obesidad.
Medicina e Investigación Universidad Autónoma del Estado de México, [S.l.], v. 11, n. 1, p. 49-58, mayo 2023.
ISSN 2594-0600.
Disponible en: <https://medicinainvestigacion.uaemex.mx/article/view/19791>. Fecha de acceso: 18 ago. 2026
doi: https://doi.org/10.36677/medicinainvestigacion.v11i1.19791.
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Esta obra está bajo licencia internacional Creative Commons Reconocimiento-NoComercial-SinObrasDerivadas 4.0.
Citas
1. World Health Organization. Obesity and overweight [Internet]. 2017 [citado 19 de agosto de 2022]. Disponible en: https://www.who.int/news-room/fact-sheets/detail/obesity-and-overweight
2. Barquera S, Rivera JA. Obesity in Mexico: rapid epidemiological transition and food industry interference in health policies. The Lancet Diabetes & Endocrinology. 1 de septiembre de 2020;8(9):746-7.
3. Swinburn BA, Sacks G, Hall KD, McPherson K, Finegood DT, Moodie ML, et al. The global obesity pandemic: shaped by global drivers and local environments. The Lancet. 27 de agosto de 2011;378(9793):804-14.
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8. Ying W, Fu W, Lee YS, Olefsky JM. The role of macrophages in obesity-associated islet inflammation and β-cell abnormalities. Nat Rev Endocrinol. febrero de 2020;16(2):81-90.
9. Caron A, Lee S, Elmquist JK, Gautron L. Leptin and brain-adipose crosstalks. Nat Rev Neurosci. 16 de febrero de 2018;19(3):153-65.
10. Roh E, Song DK, Kim MS. Emerging role of the brain in the homeostatic regulation of energy and glucose metabolism. Exp Mol Med. marzo de 2016;48(3):e216-e216.
11. Amigo I, Kowaltowski AJ. Dietary restriction in cerebral bioenergetics and redox state. Redox Biol. 2014;2:296-304.
12. Sandoval DA, Obici S, Seeley RJ. Targeting the CNS to treat type 2 diabetes. Nat Rev Drug Discov. mayo de 2009;8(5):386-98.
13. Schwartz MW, Seeley RJ, Tschöp MH, Woods SC, Morton GJ, Myers MG, et al. Cooperation between brain and islet in glucose homeostasis and diabetes. Nature. 7 de noviembre de 2013;503(7474):59-66.
14. Morton GJ, Meek TH, Schwartz MW. Neurobiology of food intake in health and disease. Nat Rev Neurosci. junio de 2014;15(6):367-78.
15. Rodríguez EM, Blázquez JL, Guerra M. The design of barriers in the hypothalamus allows the median eminence and the arcuate nucleus to enjoy private milieus: the former opens to the portal blood and the latter to the cerebrospinal fluid. Peptides. abril de 2010;31(4):757-76.
16. Kleinridders A, Könner AC, Brüning JC. CNS-targets in control of energy and glucose homeostasis. Curr Opin Pharmacol. diciembre de 2009;9(6):794-804.
17. Waterson MJ, Horvath TL. Neuronal Regulation of Energy Homeostasis: Beyond the Hypothalamus and Feeding. Cell Metab. 1 de diciembre de 2015;22(6):962-70.
18. Roh E, Kim MS. Brain Regulation of Energy Metabolism. Endocrinol Metab (Seoul). diciembre de 2016;31(4):519-24.
19. Cowley MA, Pronchuk N, Fan W, Dinulescu DM, Colmers WF, Cone RD. Integration of NPY, AGRP, and melanocortin signals in the hypothalamic paraventricular nucleus: evidence of a cellular basis for the adipostat. Neuron. septiembre de 1999;24(1):155-63.
20. Raposinho PD, Pierroz DD, Broqua P, White RB, Pedrazzini T, Aubert ML. Chronic administration of neuropeptide Y into the lateral ventricle of C57BL/6J male mice produces an obesity syndrome including hyperphagia, hyperleptinemia, insulin resistance, and hypogonadism. Mol Cell Endocrinol. 20 de diciembre de 2001;185(1-2):195-204.
21. Schwartz MW, Woods SC, Porte D, Seeley RJ, Baskin DG. Central nervous system control of food intake. Nature. 6 de abril de 2000;404(6778):661-71.
22. Luquet S, Perez FA, Hnasko TS, Palmiter RD. NPY/AgRP neurons are essential for feeding in adult mice but can be ablated in neonates. Science. 28 de octubre de 2005;310(5748):683-5.
23. Ibrahim N, Bosch MA, Smart JL, Qiu J, Rubinstein M, Rønnekleiv OK, et al. Hypothalamic proopiomelanocortin neurons are glucose responsive and express K(ATP) channels. Endocrinology. abril de 2003;144(4):1331-40.
24. Hu Z, Cha SH, Chohnan S, Lane MD. Hypothalamic malonyl-CoA as a mediator of feeding behavior. Proc Natl Acad Sci U S A. 28 de octubre de 2003;100(22):12624-9.
25. Obici S, Feng Z, Morgan K, Stein D, Karkanias G, Rossetti L. Central administration of oleic acid inhibits glucose production and food intake. Diabetes. febrero de 2002;51(2):271-5.
26. Baskin DG, Figlewicz Lattemann D, Seeley RJ, Woods SC, Porte D, Schwartz MW. Insulin and leptin: dual adiposity signals to the brain for the regulation of food intake and body weight. Brain Res. 27 de noviembre de 1999;848(1-2):114-23.
27. Elias CF, Aschkenasi C, Lee C, Kelly J, Ahima RS, Bjorbaek C, et al. Leptin differentially regulates NPY and POMC neurons projecting to the lateral hypothalamic area. Neuron. agosto de 1999;23(4):775-86.
28. Cone RD. Anatomy and regulation of the central melanocortin system. Nat Neurosci. mayo de 2005;8(5):571-8.
29. Maejima Y, Sedbazar U, Suyama S, Kohno D, Onaka T, Takano E, et al. Nesfatin-1-regulated oxytocinergic signaling in the paraventricular nucleus causes anorexia through a leptin-independent melanocortin pathway. Cell Metab. noviembre de 2009;10(5):355-65.
30. Turton MD, O’Shea D, Gunn I, Beak SA, Edwards CM, Meeran K, et al. A role for glucagon-like peptide-1 in the central regulation of feeding. Nature. 4 de enero de 1996;379(6560):69-72.
31. Parker KL, Schimmer BP. Steroidogenic factor 1: a key determinant of endocrine development and function. Endocr Rev. junio de 1997;18(3):361-77.
32. Unger TJ, Calderon GA, Bradley LC, Sena-Esteves M, Rios M. Selective deletion of Bdnf in the ventromedial and dorsomedial hypothalamus of adult mice results in hyperphagic behavior and obesity. J Neurosci. 26 de diciembre de 2007;27(52):14265-74.
33. Gray J, Yeo GSH, Cox JJ, Morton J, Adlam ALR, Keogh JM, et al. Hyperphagia, severe obesity, impaired cognitive function, and hyperactivity associated with functional loss of one copy of the brain-derived neurotrophic factor (BDNF) gene. Diabetes. diciembre de 2006;55(12):3366-71.
34. Yeo GSH, Connie Hung CC, Rochford J, Keogh J, Gray J, Sivaramakrishnan S, et al. A de novo mutation affecting human TrkB associated with severe obesity and developmental delay. Nat Neurosci. noviembre de 2004;7(11):1187-9.
35. Berridge KC, Kringelbach ML. Affective neuroscience of pleasure: reward in humans and animals. Psychopharmacology (Berl). agosto de 2008;199(3):457-80.
36. Yeo GSH, Heisler LK. Unraveling the brain regulation of appetite: lessons from genetics. Nat Neurosci. octubre de 2012;15(10):1343-9.
37. Segal-Lieberman G, Bradley RL, Kokkotou E, Carlson M, Trombly DJ, Wang X, et al. Melanin-concentrating hormone is a critical mediator of the leptin-deficient phenotype. Proc Natl Acad Sci U S A. 19 de agosto de 2003;100(17):10085-90.
38. Ludwig DS, Tritos NA, Mastaitis JW, Kulkarni R, Kokkotou E, Elmquist J, et al. Melanin-concentrating hormone overexpression in transgenic mice leads to obesity and insulin resistance. J Clin Invest. febrero de 2001;107(3):379-86.
39. Alonso-Alonso M, Woods SC, Pelchat M, Grigson PS, Stice E, Farooqi S, et al. Food reward system: current perspectives and future research needs. Nutr Rev. mayo de 2015;73(5):296-307.
40. Licinio J, Caglayan S, Ozata M, Yildiz BO, de Miranda PB, O’Kirwan F, et al. Phenotypic effects of leptin replacement on morbid obesity, diabetes mellitus, hypogonadism, and behavior in leptin-deficient adults. Proc Natl Acad Sci U S A. 30 de marzo de 2004;101(13):4531-6.
41. Obradovic M, Sudar-Milovanovic E, Soskic S, Essack M, Arya S, Stewart AJ, et al. Leptin and Obesity: Role and Clinical Implication. Front Endocrinol (Lausanne). 18 de mayo de 2021;12:585887.
42. Kwon O, Kim KW, Kim MS. Leptin signalling pathways in hypothalamic neurons. Cell Mol Life Sci. abril de 2016;73(7):1457-77.
43. van der Heijden RA, Sheedfar F, Morrison MC, Hommelberg PPH, Kor D, Kloosterhuis NJ, et al. High-fat diet induced obesity primes inflammation in adipose tissue prior to liver in C57BL/6j mice. Aging (Albany NY). abril de 2015;7(4):256-68.
44. Prentki M, Matschinsky FM, Madiraju SRM. Metabolic signaling in fuel-induced insulin secretion. Cell Metab. 6 de agosto de 2013;18(2):162-85.
45. Vettor R, Fabris R, Pagano C, Federspil G. Neuroendocrine regulation of eating behavior. J Endocrinol Invest. noviembre de 2002;25(10):836-54.
46. Könner AC, Janoschek R, Plum L, Jordan SD, Rother E, Ma X, et al. Insulin action in AgRP-expressing neurons is required for suppression of hepatic glucose production. Cell Metab. junio de 2007;5(6):438-49.
47. Hill JW, Elias CF, Fukuda M, Williams KW, Berglund ED, Holland WL, et al. Direct insulin and leptin action on pro-opiomelanocortin neurons is required for normal glucose homeostasis and fertility. Cell Metab. 7 de abril de 2010;11(4):286-97.
48. Dodd G, Descherf S, Loh K, Simonds SE, Wiede F, Balland E, et al. Leptin and insulin act on POMC neurons to promote the browning of white fat. Cell. 15 de enero de 2015;160(0):88-104.
49. Shin AC, Filatova N, Lindtner C, Chi T, Degann S, Oberlin D, et al. Insulin Receptor Signaling in POMC, but Not AgRP, Neurons Controls Adipose Tissue Insulin Action. Diabetes. junio de 2017;66(6):1560-71.
50. Andrews ZB. Central mechanisms involved in the orexigenic actions of ghrelin. Peptides. noviembre de 2011;32(11):2248-55.
51. Sobrino Crespo C, Perianes Cachero A, Puebla Jiménez L, Barrios V, Arilla Ferreiro E. Peptides and food intake. Front Endocrinol (Lausanne). 2014;5:58.
52. Richard JE, Farkas I, Anesten F, Anderberg RH, Dickson SL, Gribble FM, et al. GLP-1 receptor stimulation of the lateral parabrachial nucleus reduces food intake: neuroanatomical, electrophysiological, and behavioral evidence. Endocrinology. noviembre de 2014;155(11):4356-67.
53. Skibicka KP. The central GLP-1: implications for food and drug reward. Front Neurosci. 14 de octubre de 2013;7:181.
54. Alhadeff AL, Rupprecht LE, Hayes MR. GLP-1 neurons in the nucleus of the solitary tract project directly to the ventral tegmental area and nucleus accumbens to control for food intake. Endocrinology. febrero de 2012;153(2):647-58.
55. Choe SS, Huh JY, Hwang IJ, Kim JI, Kim JB. Adipose Tissue Remodeling: Its Role in Energy Metabolism and Metabolic Disorders. Front Endocrinol (Lausanne). 2016;7:30.
56. Zhao X, Yang Y, Sun BF, Zhao YL, Yang YG. FTO and obesity: mechanisms of association. Curr Diab Rep. 2014;14(5):486.
2. Barquera S, Rivera JA. Obesity in Mexico: rapid epidemiological transition and food industry interference in health policies. The Lancet Diabetes & Endocrinology. 1 de septiembre de 2020;8(9):746-7.
3. Swinburn BA, Sacks G, Hall KD, McPherson K, Finegood DT, Moodie ML, et al. The global obesity pandemic: shaped by global drivers and local environments. The Lancet. 27 de agosto de 2011;378(9793):804-14.
4. Secretaría de Salud, Instituto Nacional de Salud Pública, Instituto Nacional de Estadística y Geografía. Encuesta Nacional de Salud y Nutrición México 2018 | CODAJIC [Internet]. Encuesta Nacional de Salud y Nutrición. 2019 [citado 11 de agosto de 2022]. Disponible en: http://www.codajic.org/node/4182.
5. World Health Organization. Controlling the global obesity epidemic [Internet]. Nutrition and Food Safety. 2022. Disponible en: https://www.who.int/activities/controlling-the-global-obesity-epidemic
6. Parimisetty A, Dorsemans AC, Awada R, Ravanan P, Diotel N, Lefebvre d’Hellencourt C. Secret talk between adipose tissue and central nervous system via secreted factors—an emerging frontier in the neurodegenerative research. Journal of Neuroinflammation. 24 de marzo de 2016;13(1):67.
7. Thaker VV. GENETIC AND EPIGENETIC CAUSES OF OBESITY. Adolesc Med State Art Rev. 2017;28(2):379-405.
8. Ying W, Fu W, Lee YS, Olefsky JM. The role of macrophages in obesity-associated islet inflammation and β-cell abnormalities. Nat Rev Endocrinol. febrero de 2020;16(2):81-90.
9. Caron A, Lee S, Elmquist JK, Gautron L. Leptin and brain-adipose crosstalks. Nat Rev Neurosci. 16 de febrero de 2018;19(3):153-65.
10. Roh E, Song DK, Kim MS. Emerging role of the brain in the homeostatic regulation of energy and glucose metabolism. Exp Mol Med. marzo de 2016;48(3):e216-e216.
11. Amigo I, Kowaltowski AJ. Dietary restriction in cerebral bioenergetics and redox state. Redox Biol. 2014;2:296-304.
12. Sandoval DA, Obici S, Seeley RJ. Targeting the CNS to treat type 2 diabetes. Nat Rev Drug Discov. mayo de 2009;8(5):386-98.
13. Schwartz MW, Seeley RJ, Tschöp MH, Woods SC, Morton GJ, Myers MG, et al. Cooperation between brain and islet in glucose homeostasis and diabetes. Nature. 7 de noviembre de 2013;503(7474):59-66.
14. Morton GJ, Meek TH, Schwartz MW. Neurobiology of food intake in health and disease. Nat Rev Neurosci. junio de 2014;15(6):367-78.
15. Rodríguez EM, Blázquez JL, Guerra M. The design of barriers in the hypothalamus allows the median eminence and the arcuate nucleus to enjoy private milieus: the former opens to the portal blood and the latter to the cerebrospinal fluid. Peptides. abril de 2010;31(4):757-76.
16. Kleinridders A, Könner AC, Brüning JC. CNS-targets in control of energy and glucose homeostasis. Curr Opin Pharmacol. diciembre de 2009;9(6):794-804.
17. Waterson MJ, Horvath TL. Neuronal Regulation of Energy Homeostasis: Beyond the Hypothalamus and Feeding. Cell Metab. 1 de diciembre de 2015;22(6):962-70.
18. Roh E, Kim MS. Brain Regulation of Energy Metabolism. Endocrinol Metab (Seoul). diciembre de 2016;31(4):519-24.
19. Cowley MA, Pronchuk N, Fan W, Dinulescu DM, Colmers WF, Cone RD. Integration of NPY, AGRP, and melanocortin signals in the hypothalamic paraventricular nucleus: evidence of a cellular basis for the adipostat. Neuron. septiembre de 1999;24(1):155-63.
20. Raposinho PD, Pierroz DD, Broqua P, White RB, Pedrazzini T, Aubert ML. Chronic administration of neuropeptide Y into the lateral ventricle of C57BL/6J male mice produces an obesity syndrome including hyperphagia, hyperleptinemia, insulin resistance, and hypogonadism. Mol Cell Endocrinol. 20 de diciembre de 2001;185(1-2):195-204.
21. Schwartz MW, Woods SC, Porte D, Seeley RJ, Baskin DG. Central nervous system control of food intake. Nature. 6 de abril de 2000;404(6778):661-71.
22. Luquet S, Perez FA, Hnasko TS, Palmiter RD. NPY/AgRP neurons are essential for feeding in adult mice but can be ablated in neonates. Science. 28 de octubre de 2005;310(5748):683-5.
23. Ibrahim N, Bosch MA, Smart JL, Qiu J, Rubinstein M, Rønnekleiv OK, et al. Hypothalamic proopiomelanocortin neurons are glucose responsive and express K(ATP) channels. Endocrinology. abril de 2003;144(4):1331-40.
24. Hu Z, Cha SH, Chohnan S, Lane MD. Hypothalamic malonyl-CoA as a mediator of feeding behavior. Proc Natl Acad Sci U S A. 28 de octubre de 2003;100(22):12624-9.
25. Obici S, Feng Z, Morgan K, Stein D, Karkanias G, Rossetti L. Central administration of oleic acid inhibits glucose production and food intake. Diabetes. febrero de 2002;51(2):271-5.
26. Baskin DG, Figlewicz Lattemann D, Seeley RJ, Woods SC, Porte D, Schwartz MW. Insulin and leptin: dual adiposity signals to the brain for the regulation of food intake and body weight. Brain Res. 27 de noviembre de 1999;848(1-2):114-23.
27. Elias CF, Aschkenasi C, Lee C, Kelly J, Ahima RS, Bjorbaek C, et al. Leptin differentially regulates NPY and POMC neurons projecting to the lateral hypothalamic area. Neuron. agosto de 1999;23(4):775-86.
28. Cone RD. Anatomy and regulation of the central melanocortin system. Nat Neurosci. mayo de 2005;8(5):571-8.
29. Maejima Y, Sedbazar U, Suyama S, Kohno D, Onaka T, Takano E, et al. Nesfatin-1-regulated oxytocinergic signaling in the paraventricular nucleus causes anorexia through a leptin-independent melanocortin pathway. Cell Metab. noviembre de 2009;10(5):355-65.
30. Turton MD, O’Shea D, Gunn I, Beak SA, Edwards CM, Meeran K, et al. A role for glucagon-like peptide-1 in the central regulation of feeding. Nature. 4 de enero de 1996;379(6560):69-72.
31. Parker KL, Schimmer BP. Steroidogenic factor 1: a key determinant of endocrine development and function. Endocr Rev. junio de 1997;18(3):361-77.
32. Unger TJ, Calderon GA, Bradley LC, Sena-Esteves M, Rios M. Selective deletion of Bdnf in the ventromedial and dorsomedial hypothalamus of adult mice results in hyperphagic behavior and obesity. J Neurosci. 26 de diciembre de 2007;27(52):14265-74.
33. Gray J, Yeo GSH, Cox JJ, Morton J, Adlam ALR, Keogh JM, et al. Hyperphagia, severe obesity, impaired cognitive function, and hyperactivity associated with functional loss of one copy of the brain-derived neurotrophic factor (BDNF) gene. Diabetes. diciembre de 2006;55(12):3366-71.
34. Yeo GSH, Connie Hung CC, Rochford J, Keogh J, Gray J, Sivaramakrishnan S, et al. A de novo mutation affecting human TrkB associated with severe obesity and developmental delay. Nat Neurosci. noviembre de 2004;7(11):1187-9.
35. Berridge KC, Kringelbach ML. Affective neuroscience of pleasure: reward in humans and animals. Psychopharmacology (Berl). agosto de 2008;199(3):457-80.
36. Yeo GSH, Heisler LK. Unraveling the brain regulation of appetite: lessons from genetics. Nat Neurosci. octubre de 2012;15(10):1343-9.
37. Segal-Lieberman G, Bradley RL, Kokkotou E, Carlson M, Trombly DJ, Wang X, et al. Melanin-concentrating hormone is a critical mediator of the leptin-deficient phenotype. Proc Natl Acad Sci U S A. 19 de agosto de 2003;100(17):10085-90.
38. Ludwig DS, Tritos NA, Mastaitis JW, Kulkarni R, Kokkotou E, Elmquist J, et al. Melanin-concentrating hormone overexpression in transgenic mice leads to obesity and insulin resistance. J Clin Invest. febrero de 2001;107(3):379-86.
39. Alonso-Alonso M, Woods SC, Pelchat M, Grigson PS, Stice E, Farooqi S, et al. Food reward system: current perspectives and future research needs. Nutr Rev. mayo de 2015;73(5):296-307.
40. Licinio J, Caglayan S, Ozata M, Yildiz BO, de Miranda PB, O’Kirwan F, et al. Phenotypic effects of leptin replacement on morbid obesity, diabetes mellitus, hypogonadism, and behavior in leptin-deficient adults. Proc Natl Acad Sci U S A. 30 de marzo de 2004;101(13):4531-6.
41. Obradovic M, Sudar-Milovanovic E, Soskic S, Essack M, Arya S, Stewart AJ, et al. Leptin and Obesity: Role and Clinical Implication. Front Endocrinol (Lausanne). 18 de mayo de 2021;12:585887.
42. Kwon O, Kim KW, Kim MS. Leptin signalling pathways in hypothalamic neurons. Cell Mol Life Sci. abril de 2016;73(7):1457-77.
43. van der Heijden RA, Sheedfar F, Morrison MC, Hommelberg PPH, Kor D, Kloosterhuis NJ, et al. High-fat diet induced obesity primes inflammation in adipose tissue prior to liver in C57BL/6j mice. Aging (Albany NY). abril de 2015;7(4):256-68.
44. Prentki M, Matschinsky FM, Madiraju SRM. Metabolic signaling in fuel-induced insulin secretion. Cell Metab. 6 de agosto de 2013;18(2):162-85.
45. Vettor R, Fabris R, Pagano C, Federspil G. Neuroendocrine regulation of eating behavior. J Endocrinol Invest. noviembre de 2002;25(10):836-54.
46. Könner AC, Janoschek R, Plum L, Jordan SD, Rother E, Ma X, et al. Insulin action in AgRP-expressing neurons is required for suppression of hepatic glucose production. Cell Metab. junio de 2007;5(6):438-49.
47. Hill JW, Elias CF, Fukuda M, Williams KW, Berglund ED, Holland WL, et al. Direct insulin and leptin action on pro-opiomelanocortin neurons is required for normal glucose homeostasis and fertility. Cell Metab. 7 de abril de 2010;11(4):286-97.
48. Dodd G, Descherf S, Loh K, Simonds SE, Wiede F, Balland E, et al. Leptin and insulin act on POMC neurons to promote the browning of white fat. Cell. 15 de enero de 2015;160(0):88-104.
49. Shin AC, Filatova N, Lindtner C, Chi T, Degann S, Oberlin D, et al. Insulin Receptor Signaling in POMC, but Not AgRP, Neurons Controls Adipose Tissue Insulin Action. Diabetes. junio de 2017;66(6):1560-71.
50. Andrews ZB. Central mechanisms involved in the orexigenic actions of ghrelin. Peptides. noviembre de 2011;32(11):2248-55.
51. Sobrino Crespo C, Perianes Cachero A, Puebla Jiménez L, Barrios V, Arilla Ferreiro E. Peptides and food intake. Front Endocrinol (Lausanne). 2014;5:58.
52. Richard JE, Farkas I, Anesten F, Anderberg RH, Dickson SL, Gribble FM, et al. GLP-1 receptor stimulation of the lateral parabrachial nucleus reduces food intake: neuroanatomical, electrophysiological, and behavioral evidence. Endocrinology. noviembre de 2014;155(11):4356-67.
53. Skibicka KP. The central GLP-1: implications for food and drug reward. Front Neurosci. 14 de octubre de 2013;7:181.
54. Alhadeff AL, Rupprecht LE, Hayes MR. GLP-1 neurons in the nucleus of the solitary tract project directly to the ventral tegmental area and nucleus accumbens to control for food intake. Endocrinology. febrero de 2012;153(2):647-58.
55. Choe SS, Huh JY, Hwang IJ, Kim JI, Kim JB. Adipose Tissue Remodeling: Its Role in Energy Metabolism and Metabolic Disorders. Front Endocrinol (Lausanne). 2016;7:30.
56. Zhao X, Yang Y, Sun BF, Zhao YL, Yang YG. FTO and obesity: mechanisms of association. Curr Diab Rep. 2014;14(5):486.