Does Nutrient Sensing Determine How We “See” Food?

Current Diabetes Reports

Volumn 15, Issue 6, 2015, Pages

  Hamr, Sophie C ^a,b   Wang, Beini ^a,b   Swartz, Timothy D ^c,d   Duca, Frank A ^b  

^a UNIVERSITY OF TORONTO   (Canada)

^b UNIVERSITY HEALTH NETWORK   (Canada)

^c INSTITUT COCHIN   (France)

^d DANONE RESEARCH   (France)

Author keywords

Food intake; Glucose homeostasis; Gut peptides; Hypothalamus; Intestine

Indexed keywords

CARBOHYDRATE; LIPID; PROTEIN;

CALORIC INTAKE; CELLULAR, SUBCELLULAR AND MOLECULAR BIOLOGICAL PHENOMENA AND FUNCTIONS; ENERGY BALANCE; FOOD INTAKE; FOOD PREFERENCE; GLUCOSE HOMEOSTASIS; HUMAN; HYPOTHALAMUS; INTESTINE WALL; NON INSULIN DEPENDENT DIABETES MELLITUS; NUTRIENT SENSING; OBESITY; REVIEW; REWARD; RHOMBENCEPHALON; BRAIN; CARBOHYDRATE METABOLISM; ENERGY METABOLISM; HOMEOSTASIS; INTESTINE; LIPID METABOLISM; METABOLISM; NUTRITION; PHYSIOLOGY;

BRAIN; CARBOHYDRATE METABOLISM; ENERGY METABOLISM; HOMEOSTASIS; HUMANS; INTESTINES; LIPID METABOLISM; NUTRITION PROCESSES; PROTEINS;

EID: 84929000265     PISSN: 15344827     EISSN: 15390829     Source Type: Journal    
DOI: 10.1007/s11892-015-0604-7     Document Type: Review

References (115)

1. Ritter RC. Gastrointestinal mechanisms of satiation for food. Physiol Behav. 2004;81(2):249–73.
2. Duca FA, Yue JT. Fatty acid sensing in the gut and the hypothalamus: in vivo and in vitro perspectives. Mol Cell Endocrinol. 2014.
3. Sidhu SS, Thompson DG, Warhurst G, et al. Fatty acid-induced cholecystokinin secretion and changes in intracellular Ca2+ in two enteroendocrine cell lines, STC-1 and GLUTag. J Physiol. 2000;528(Pt 1):165–76.
4. Liou AP, Lu X, Sei Y, et al. The G-protein-coupled receptor GPR40 directly mediates long-chain fatty acid-induced secretion of cholecystokinin. Gastroenterology. 2011;140(3):903–12.
5. Powley TL, Spaulding RA, Haglof SA. Vagal afferent innervation of the proximal gastrointestinal tract mucosa: chemoreceptor and mechanoreceptor architecture. J Comp Neurol. 2011;519(4):644–60.
6. Randich A, Tyler WJ, Cox JE, et al. Responses of celiac and cervical vagal afferents to infusions of lipids in the jejunum or ileum of the rat. Am J Physiol Regul Integr Comp Physiol. 2000;278(1):R34–43.
7. Webster WA, Beyak MJ. The long chain fatty acid oleate activates mouse intestinal afferent nerves in vitro. Can J Physiol Pharmacol. 2013;91(5):375–9.
8. Ritter RC, Covasa M, Matson CA. Cholecystokinin: proofs and prospects for involvement in control of food intake and body weight. Neuropeptides. 1999;33(5):387–99.
9. Edfalk S, Steneberg P, Edlund H. Gpr40 is expressed in enteroendocrine cells and mediates free fatty acid stimulation of incretin secretion. Diabetes. 2008;57(9):2280–7.
10. Hirasawa A, Tsumaya K, Awaji T, et al. Free fatty acids regulate gut incretin glucagon-like peptide-1 secretion through GPR120. Nat Med. 2005;11(1):90–4.
11. Sundaresan S, Shahid R, Riehl TE, et al. CD36-dependent signaling mediates fatty acid-induced gut release of secretin and cholecystokinin. FASEB J. 2013;27(3):1191–202. This study is the first to show that CCK release is partially mediated by CD36 in vivo, elucidating EEC lipid sensing mechanisms upstream of lipid-induced CCK release.
12. Cote CD, Zadeh-Tahmasebi M, Rasmussen BA, et al. Hormonal signaling in the gut. J Biol Chem. 2014;289(17):11642–9.
13. Dailey MJ, Moghadam AA, Moran TH. Jejunal linoleic acid infusions require GLP-1 receptor signaling to inhibit food intake: implications for the effectiveness of Roux-en-Y gastric bypass. Am J Physiol Endocrinol Metab. 2011;301(6):E1184–90.
14. Burton-Freeman B, Gietzen DW, Schneeman BO. Meal pattern analysis to investigate the satiating potential of fat, carbohydrate, and protein in rats. Am J Physiol. 1997;273(6 Pt 2):R1916–22.
15. Breen DM, Rasmussen BA, Kokorovic A, et al. Jejunal nutrient sensing is required for duodenal-jejunal bypass surgery to rapidly lower glucose concentrations in uncontrolled diabetes. Nat Med. 2012;18(6):950–5. This study shows for the first time that jejunal glucose and lipid sensing mechanisms lower glucose production and that these jejunal nutrient sensing mechanisms are necessary for DJB surgery to improve glycemia in diabetic rodents, highlighting important therapeutic relevance for intestinal nutrient sensing mechanisms.
16. Holst JJ. The physiology of glucagon-like peptide 1. Physiol Rev. 2007;87(4):1409–39.
17. Hayes MR. Neuronal and intracellular signaling pathways mediating GLP-1 energy balance and glycemic effects. Physiol Behav. 2012;106(3):413–6.
18. Williams DL, Baskin DG, Schwartz MW. Evidence that intestinal glucagon-like peptide-1 plays a physiological role in satiety. Endocrinology. 2009;150(4):1680–7.
19. Theodorakis MJ, Carlson O, Michopoulos S, et al. Human duodenal enteroendocrine cells: source of both incretin peptides, GLP-1 and GIP. Am J Physiol Endocrinol Metab. 2006;290(3):E550–9.
20. Jang HJ, Kokrashvili Z, Theodorakis MJ, et al. Gut-expressed gustducin and taste receptors regulate secretion of glucagon-like peptide-1. Proc Natl Acad Sci U S A. 2007;104(38):15069–74.
21. Parker HE, Habib AM, Rogers GJ, et al. Nutrient-dependent secretion of glucose-dependent insulinotropic polypeptide from primary murine K cells. Diabetologia. 2009;52(2):289–98.
22. Tolhurst G, Reimann F, Gribble FM. Intestinal sensing of nutrients. Handb Exp Pharmacol. 2012;209:309–35.
23. Reimann F, Habib AM, Tolhurst G, et al. Glucose sensing in L cells: a primary cell study. Cell Metab. 2008;8(6):532–9.
24. Moriya R, Shirakura T, Ito J, et al. Activation of sodium-glucose cotransporter 1 ameliorates hyperglycemia by mediating incretin secretion in mice. Am J Physiol Endocrinol Metab. 2009;297(6):E1358–65.
25. Gorboulev V, Schurmann A, Vallon V, et al. Na(+)-D-glucose cotransporter SGLT1 is pivotal for intestinal glucose absorption and glucose-dependent incretin secretion. Diabetes. 2012;61(1):187–96. This study highlights SGLT1 glucose transporter as a potential mediator in glucose-induced incretin secretion.
26. Perez C, Lucas F, Sclafani A. Devazepide, a CCK(A) antagonist, attenuates the satiating but not the preference conditioning effects of intestinal carbohydrate infusions in rats. Pharmacol Biochem Behav. 1998;59(2):451–7.
27. Covasa M, Ritter RC. Attenuated satiation response to intestinal nutrients in rats that do not express CCK-A receptors. Peptides. 2001;22(8):1339–48.
28. Yox DP, Ritter RC. Capsaicin attenuates suppression of sham feeding induced by intestinal nutrients. Am J Physiol. 1988;255(4 Pt 2):R569–74.
29. Meyer JH, Hlinka M, Tabrizi Y, et al. Chemical specificities and intestinal distributions of nutrient-driven satiety. Am J Physiol. 1998;275(4 Pt 2):R1293–307.
30. Liou AP, Chavez DI, Espero E, et al. Protein hydrolysate-induced cholecystokinin secretion from enteroendocrine cells is indirectly mediated by the intestinal oligopeptide transporter PepT1. Am J Physiol Gastrointest Liver Physiol. 2011;300(5):G895–902.
31. Darcel NP, Liou AP, Tome D, et al. Activation of vagal afferents in the rat duodenum by protein digests requires PepT1. J Nutr. 2005;135(6):1491–5.
32. Nemoz-Gaillard E, Bernard C, Abello J, et al. Regulation of cholecystokinin secretion by peptones and peptidomimetic antibiotics in STC-1 cells. Endocrinology. 1998;139(3):932–8.
33. Liou AP, Sei Y, Zhao X, et al. The extracellular calcium-sensing receptor is required for cholecystokinin secretion in response to L-phenylalanine in acutely isolated intestinal I cells. Am J Physiol Gastrointest Liver Physiol. 2011;300(4):G538–46.
34. Blouet C, Mariotti F, Azzout-Marniche D, et al. The reduced energy intake of rats fed a high-protein low-carbohydrate diet explains the lower fat deposition, but macronutrient substitution accounts for the improved glycemic control. J Nutr. 2006;136(7):1849–54.
35. Gannon MC, Nuttall FQ, Saeed A, et al. An increase in dietary protein improves the blood glucose response in persons with type 2 diabetes. Am J Clin Nutr. 2003;78(4):734–41.
36. Akhavan T, Luhovyy BL, Brown PH, et al. Effect of premeal consumption of whey protein and its hydrolysate on food intake and postmeal glycemia and insulin responses in young adults. Am J Clin Nutr. 2010;91(4):966–75.
37. Douglas BR, Woutersen RA, Jansen JB, et al. The influence of different nutrients on plasma cholecystokinin levels in the rat. Experientia. 1988;44(1):21–3.
38. van der Klaauw AA, Keogh JM, Henning E, et al. High protein intake stimulates postprandial GLP1 and PYY release. Obesity (Silver Spring). 2013;21(8):1602–7.
39. Seimon RV, Feltrin KL, Meyer JH, et al. Effects of varying combinations of intraduodenal lipid and carbohydrate on antropyloroduodenal motility, hormone release, and appetite in healthy males. Am J Physiol Regul Integr Comp Physiol. 2009;296(4):R912–20.
40. Ryan AT, Luscombe-Marsh ND, Saies AA, et al. Effects of intraduodenal lipid and protein on gut motility and hormone release, glycemia, appetite, and energy intake in lean men. Am J Clin Nutr. 2013;98(2):300–11. This study assesses the gut peptide response to intraduodenal nutrient infusion in human subjects, as opposed to the numerous studies of nutrient infusion in rodents. Further, this study shows important differences gut peptide responses to different types of nutrients.
41. Brennan IM, Luscombe-Marsh ND, Seimon RV, et al. Effects of fat, protein, and carbohydrate and protein load on appetite, plasma cholecystokinin, peptide YY, and ghrelin, and energy intake in lean and obese men. Am J Physiol Gastrointest Liver Physiol. 2012;303(1):G129–40.
42. Lam TK, Pocai A, Gutierrez-Juarez R, et al. Hypothalamic sensing of circulating fatty acids is required for glucose homeostasis. Nat Med. 2005;11(3):320–7.
43. Obici S, Feng Z, Morgan K, et al. Central administration of oleic acid inhibits glucose production and food intake. Diabetes. 2002;51(2):271–5.
44. Wang R, Cruciani-Guglielmacci C, Migrenne S, et al. Effects of oleic acid on distinct populations of neurons in the hypothalamic arcuate nucleus are dependent on extracellular glucose levels. J Neurophysiol. 2006;95(3):1491–8.
45. Jo YH, Su Y, Gutierrez-Juarez R, et al. Oleic acid directly regulates POMC neuron excitability in the hypothalamus. J Neurophysiol. 2009;101(5):2305–16.
46. Picard A, Rouch C, Kassis N, et al. Hippocampal lipoprotein lipase regulates energy balance in rodents. Mol Metab. 2014;3(2):167–76. This study is the first to identify that the hippocampus can sense lipids via LPL activity to regulate energy homeostasis, supporting a role for extra-hypothalamic regions to sense nutrients.
47. Le Foll C, Dunn-Meynell A, Musatov S, et al. FAT/CD36: a major regulator of neuronal fatty acid sensing and energy homeostasis in rats and mice. Diabetes. 2013;62(8):2709–16.
48. Moulle VS, Le Foll C, Philippe E, et al. Fatty acid transporter CD36 mediates hypothalamic effect of fatty acids on food intake in rats. PLoS One. 2013;8(9):e74021.
49. Wang H, Astarita G, Taussig MD, et al. Deficiency of lipoprotein lipase in neurons modifies the regulation of energy balance and leads to obesity. Cell Metab. 2011;13(1):105–13.
50. Obici S, Feng Z, Arduini A, et al. Inhibition of hypothalamic carnitine palmitoyltransferase-1 decreases food intake and glucose production. Nat Med. 2003;9(6):756–61.
51. Ross R, Wang PY, Chari M, et al. Hypothalamic protein kinase C regulates glucose production. Diabetes. 2008;57(8):2061–5.
52. Guzman M, Blazquez C. Is there an astrocyte-neuron ketone body shuttle? Trends Endocrinol Metab. 2001;12(4):169–73.
53. Auestad N, Korsak RA, Morrow JW, et al. Fatty acid oxidation and ketogenesis by astrocytes in primary culture. J Neurochem. 1991;56(4):1376–86.
54. Schonfeld P, Reiser G. Why does brain metabolism not favor burning of fatty acids to provide energy? Reflections on disadvantages of the use of free fatty acids as fuel for brain. J Cereb Blood Flow Metab. 2013;33(10):1493–9.
55. Le Foll C, Irani BG, Magnan C, et al. Characteristics and mechanisms of hypothalamic neuronal fatty acid sensing. Am J Physiol Regul Integr Comp Physiol. 2009;297(3):R655–64.
56. Thorens B. Sensing of glucose in the brain. Handb Exp Pharmacol. 2012;209:277–94.
57. Kurata K, Fujimoto K, Sakata T, et al. D-glucose suppression of eating after intra-third ventricle infusion in rat. Physiol Behav. 1986;37(4):615–20.
58. Lam TK, Gutierrez-Juarez R, Pocai A, et al. Regulation of blood glucose by hypothalamic pyruvate metabolism. Science. 2005;309(5736):943–7.
59. Borg WP, Sherwin RS, During MJ, et al. Local ventromedial hypothalamus glucopenia triggers counterregulatory hormone release. Diabetes. 1995;44(2):180–4.
60. Ritter S, Dinh TT, Zhang Y. Localization of hindbrain glucoreceptive sites controlling food intake and blood glucose. Brain Res. 2000;856(1–2):37–47.
61. Edmonds BK, Edwards GL. Dorsomedial hindbrain participation in glucoprivic feeding response to 2DG but not 2DG-induced hyperglycemia or activation of the HPA axis. Brain Res. 1998;801(1–2):21–8.
62. Ritter RC, Slusser PG, Stone S. Glucoreceptors controlling feeding and blood glucose: location in the hindbrain. Science. 1981;213(4506):451–2.
63. Ibrahim N, Bosch MA, Smart JL, et al. Hypothalamic proopiomelanocortin neurons are glucose responsive and express K(ATP) channels. Endocrinology. 2003;144(4):1331–40.
64. Muroya S, Yada T, Shioda S, et al. Glucose-sensitive neurons in the rat arcuate nucleus contain neuropeptide Y. Neurosci Lett. 1999;264(1–3):113–6.
65. Leloup C, Arluison M, Lepetit N, et al. Glucose transporter 2 (GLUT 2): expression in specific brain nuclei. Brain Res. 1994;638(1–2):221–6.
66. Bady I, Marty N, Dallaporta M, et al. Evidence from glut2-null mice that glucose is a critical physiological regulator of feeding. Diabetes. 2006;55(4):988–95.
67. Mounien L, Marty N, Tarussio D, et al. Glut2-dependent glucose-sensing controls thermoregulation by enhancing the leptin sensitivity of NPY and POMC neurons. FASEB J. 2010;24(6):1747–58.
68. Lamy CM, Sanno H, Labouebe G, et al. Hypoglycemia-activated GLUT2 neurons of the nucleus tractus solitarius stimulate vagal activity and glucagon secretion. Cell Metab. 2014;19(3):527–38. This study characterizes a population of glucose-inhibited GLUT2 neurons in the NTS that sense hypoglycemia to trigger glucagon secretion. These results could help elucidate mechanisms underlying a defective counterregulatory response in insulin-treated diabetes.
69. Dunn-Meynell AA, Routh VH, Kang L, et al. Glucokinase is the likely mediator of glucosensing in both glucose-excited and glucose-inhibited central neurons. Diabetes. 2002;51(7):2056–65.
70. Stanley S, Domingos AI, Kelly L, et al. Profiling of glucose-sensing neurons reveals that GHRH neurons are activated by hypoglycemia. Cell Metab. 2013;18(4):596–607.
71. Kang L, Dunn-Meynell AA, Routh VH, et al. Glucokinase is a critical regulator of ventromedial hypothalamic neuronal glucosensing. Diabetes. 2006;55(2):412–20.
72. Levin BE, Becker TC, Eiki J, et al. Ventromedial hypothalamic glucokinase is an important mediator of the counterregulatory response to insulin-induced hypoglycemia. Diabetes. 2008;57(5):1371–9.
73. Karschin A, Brockhaus J, Ballanyi K. KATP channel formation by the sulphonylurea receptors SUR1 with Kir6.2 subunits in rat dorsal vagal neurons in situ. J Physiol. 1998;509(Pt 2):339–46.
74. Miki T, Liss B, Minami K, et al. ATP-sensitive K+ channels in the hypothalamus are essential for the maintenance of glucose homeostasis. Nat Neurosci. 2001;4(5):507–12.
75. Fioramonti X, Lorsignol A, Taupignon A, et al. A new ATP-sensitive K+ channel-independent mechanism is involved in glucose-excited neurons of mouse arcuate nucleus. Diabetes. 2004;53(11):2767–75.
76. O'Malley D, Reimann F, Simpson AK, et al. Sodium-coupled glucose cotransporters contribute to hypothalamic glucose sensing. Diabetes. 2006;55(12):3381–6.
77. Ren X, Zhou L, Terwilliger R, et al. Sweet taste signaling functions as a hypothalamic glucose sensor. Front Integr Neurosci. 2009;3:12.
78. Pellerin L, Magistretti PJ. Sweet sixteen for ANLS. J Cereb Blood Flow Metab. 2012;32(7):1152–66.
79. Marty N, Dallaporta M, Foretz M, et al. Regulation of glucagon secretion by glucose transporter type 2 (glut2) and astrocyte-dependent glucose sensors. J Clin Invest. 2005;115(12):3545–53.
80. Cota D, Proulx K, Smith KA, et al. Hypothalamic mTOR signaling regulates food intake. Science. 2006;312(5775):927–30.
81. Blouet C, Jo YH, Li X, et al. Mediobasal hypothalamic leucine sensing regulates food intake through activation of a hypothalamus-brainstem circuit. J Neurosci. 2009;29(26):8302–11.
82. Blouet C, Schwartz GJ. Brainstem nutrient sensing in the nucleus of the solitary tract inhibits feeding. Cell Metab. 2012;16(5):579–87. This study shows that the NTS can sense a postprandial concentration of leucine to lower food intake, and establishes the NTS as an important integrator of diverse fuel-related signals to regulate energy balance.
83. Su Y, Lam TK, He W, et al. Hypothalamic leucine metabolism regulates liver glucose production. Diabetes. 2012;61(1):85–93. This study highlights a novel mechanism of leucine sensing that lowers glucose production, involving the metabolism of leucine rather than activation of the mTOR pathway.
84. Sclafani A, Zukerman S, Ackroff K. Fructose and glucose conditioned preferences in FVB mice: strain differences in post-oral sugar appetition. Am J Physiol Regul Integr Comp Physiol. 2014:ajpregu 00312 2014.
85. Sclafani A, Fanizza LJ, Azzara AV. Conditioned flavor avoidance, preference, and indifference produced by intragastric infusions of galactose, glucose, and fructose in rats. Physiol Behav. 1999;67(2):227–34.
86. Zukerman S, Ackroff K, Sclafani A. Rapid post-oral stimulation of intake and flavor conditioning by glucose and fat in the mouse. Am J Physiol Regul Integr Comp Physiol. 2011;301(6):R1635–47.
87. Myers KP. Robust preference for a flavor paired with intragastric glucose acquired in a single trial. Appetite. 2007;48(1):123–7.
88. Tellez LA, Medina S, Han W, et al. A gut lipid messenger links excess dietary fat to dopamine deficiency. Science. 2013;341(6147):800–2. This study links intestinal nutrient sensing mechanism with central food reward pathways.
89. Sclafani A, Ackroff K, Schwartz GJ. Selective effects of vagal deafferentation and celiac-superior mesenteric ganglionectomy on the reinforcing and satiating action of intestinal nutrients. Physiol Behav. 2003;78(2):285–94.
90. Tsurugizawa T, Uematsu A, Uneyama H, et al. Blood oxygenation level-dependent response to intragastric load of corn oil emulsion in conscious rats. Neuroreport. 2009;20(18):1625–9.
91. Otsubo H, Kondoh T, Shibata M, et al. Induction of Fos expression in the rat forebrain after intragastric administration of monosodium L-glutamate, glucose and NaCl. Neuroscience. 2011;196:97–103.
92. Tsurugizawa T, Uematsu A, Nakamura E, et al. Mechanisms of neural response to gastrointestinal nutritive stimuli: the gut-brain axis. Gastroenterology. 2009;137(1):262–73.
93. Yiin YM, Ackroff K, Sclafani A. Flavor preferences conditioned by intragastric nutrient infusions in food restricted and free-feeding rats. Physiol Behav. 2005;84(2):217–31.
94. Sclafani A, Glass DS, Margolskee RF, et al. Gut T1R3 sweet taste receptors do not mediate sucrose-conditioned flavor preferences in mice. Am J Physiol Regul Integr Comp Physiol. 2010;299(6):R1643–50.
95. Sclafani A, Ackroff K, Abumrad NA. CD36 gene deletion reduces fat preference and intake but not post-oral fat conditioning in mice. Am J Physiol Regul Integr Comp Physiol. 2007;293(5):R1823–32.
96. Zukerman S, Ackroff K, Sclafani A. Post-oral appetite stimulation by sugars and nonmetabolizable sugar analogs. Am J Physiol Regul Integr Comp Physiol. 2013;305(7):R840–53.
97. Ackroff K, Sclafani A. Post-oral fat stimulation of intake and conditioned flavor preference in C57BL/6 J mice: a concentration-response study. Physiol Behav. 2014;129:64–72.
98. Ackroff K, Rozental D, Sclafani A. Ethanol-conditioned flavor preferences compared with sugar- and fat-conditioned preferences in rats. Physiol Behav. 2004;81(4):699–713.
99. Kanoski SE, Alhadeff AL, Fortin SM, et al. Leptin signaling in the medial nucleus tractus solitarius reduces food seeking and willingness to work for food. Neuropsychopharmacology. 2014;39(3):605–13.
100. Perez C, Sclafani A. Cholecystokinin conditions flavor preferences in rats. Am J Physiol. 1991;260(1 Pt 2):R179–85.
101. Ackroff K, Touzani K, Peets TK, et al. Flavor preferences conditioned by intragastric fructose and glucose: differences in reinforcement potency. Physiol Behav. 2001;72(5):691–703.
102. Ackroff K, Sclafani A. Flavor preferences conditioned by intragastric infusion of ethanol in rats. Pharmacol Biochem Behav. 2001;68(2):327–38.
103. Ackroff K, Dym C, Yiin YM, et al. Rapid acquisition of conditioned flavor preferences in rats. Physiol Behav. 2009;97(3–4):406–13.
104. Lucas F, Ackroff K, Sclafani A. High-fat diet preference and overeating mediated by postingestive factors in rats. Am J Physiol. 1998;275(5 Pt 2):R1511–22.
105. Sclafani A, Zukerman S, Ackroff K. GPR40 and GPR120 fatty acid sensors are critical for postoral but not oral mediation of fat preferences in the mouse. Am J Physiol Regul Integr Comp Physiol. 2013;305(12):R1490–7. This study demonstrates that mechanisms involved in postoral nutrient conditioning and prefence differ from those involved in nutrient-induced satiety.
106. Ren X, Ferreira JG, Zhou L, et al. Nutrient selection in the absence of taste receptor signaling. J Neurosci. 2010;30(23):8012–23.
107. Oliveira-Maia AJ, Roberts CD, Walker QD, et al. Intravascular food reward. PLoS One. 2011;6(9):e24992.
108. Cansell C, Castel J, Denis RG, et al. Dietary triglycerides act on mesolimbic structures to regulate the rewarding and motivational aspects of feeding. Mol Psychiatry. 2014;19(10):1095–105.
109. Duca FA, Sakar Y, Covasa M. The modulatory role of high fat feeding on gastrointestinal signals in obesity. J Nutr Biochem. 2013;24(10):1663–77.
110. Parton LE, Ye CP, Coppari R, et al. Glucose sensing by POMC neurons regulates glucose homeostasis and is impaired in obesity. Nature. 2007;449(7159):228–32.
111. Murray S, Tulloch A, Gold MS, et al. Hormonal and neural mechanisms of food reward, eating behaviour and obesity. Nat Rev Endocrinol. 2014;10(9):540–52.
112. Pothos EN, Creese I, Hoebel BG. Restricted eating with weight loss selectively decreases extracellular dopamine in the nucleus accumbens and alters dopamine response to amphetamine, morphine, and food intake. J Neurosci. 1995;15(10):6640–50.
113. Geiger BM, Haburcak M, Avena NM, et al. Deficits of mesolimbic dopamine neurotransmission in rat dietary obesity. Neuroscience. 2009;159(4):1193–9.
114. Falken Y, Hellstrom PM, Holst JJ, et al. Changes in glucose homeostasis after Roux-en-Y gastric bypass surgery for obesity at day three, two months, and one year after surgery: role of gut peptides. J Clin Endocrinol Metab. 2011;96(7):2227–35.
115. Scholtz S, Miras AD, Chhina N, et al. Obese patients after gastric bypass surgery have lower brain-hedonic responses to food than after gastric banding. Gut. 2014;63(6):891–902. This study demonstrates the impact of gastric bypass surgery on central food reward.