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The Role of Diet in Inflammation and Metabolic Syndrome

  • Chapter
Metabolic Syndrome and Complications of Pregnancy

Abstract

The human species has evolved intricate control systems to manage the intake and storage of nutrients to increase the chances for successful survival and the procreation of the next generation. However, these complex communication systems can be disturbed by increased levels of inflammation leading to metabolic defects (obesity, metabolic syndrome, and diabetes) that can make successful procreation difficult, and more ominously these metabolic defects can possibly be transmitted to the next generation via fetal programming. The purpose of this opening chapter is to present an overview of how diet-induced inflammation can lead eventually to metabolic syndrome that can have an adverse effect on pregnancy.

Inflammation is easy to define but complex to understand at the molecular level. The same is true for insulin resistance. Nonetheless, cellular inflammation induced by hypothalamic and adipose tissue damage that results from a wide variety of dietary factors appears to be a key to understanding and therefore reversing the wide range of the adverse metabolic consequences of insulin resistance.

It appears that insulin resistance starts in the hypothalamus causing a disruption in the balance of satiety and hunger signals. This leads to overconsumption of calories. Although excess calories can be theoretically stored safety in the adipose tissue, as the inflammation increases in this organ and insulin resistance develops in the fat cells, the ability to safely store excess fat is compromised. One of the consequences of insulin resistance in the adipose tissue is that excess fat is released into the bloodstream and is sequestered by other organs (liver and skeletal muscles) that are not equipped to safely store this excess fat. This is the start of lipotoxicity. With increased lipotoxicity, the metabolism and energy generation by the body become compromised, and the development of chronic diseases becomes accelerated.

Since insulin resistance is primarily caused by the diet, it can also be reversed by the diet, especially an anti-inflammatory diet, as will be discussed later in this book.

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References

  1. Odegaard JI, Chawla A. Pleiotropic actions of insulin resistance and inflammation in metabolic homeostasis. Science. 2013;339:172–7.

    CAS  PubMed Central  PubMed  Google Scholar 

  2. Zeyda M, Stulnig TM. Obesity, inflammation, and insulin resistance–a mini-review. Gerontology. 2009;55(4):379–86.

    CAS  PubMed  Google Scholar 

  3. de Luca C, Olefsky JM. Inflammation and insulin resistance. FEBS Lett. 2008;582(1):97–105.

    PubMed Central  PubMed  Google Scholar 

  4. Gregor MF, Hotamistigli GS. Inflammatory mechanisms in obesity. Ann Rev Immunol. 2011;29:415–45.

    CAS  Google Scholar 

  5. Spite M, Claria J, Serhan CN. Resolvins, specialized proresolving lipid mediators, and their potential roles in metabolic diseases. Cell Metab. 2014;19(1):21–36.

    CAS  PubMed Central  PubMed  Google Scholar 

  6. Brenner RR. Nutritional and hormonal factors influencing desaturation of essential fatty acids. Prog Lipid Res. 1981;20:41–7.

    CAS  PubMed  Google Scholar 

  7. Kratsovnik E, Bromberg Y, Sperling O, Zoref-Shani E. Oxidative stress activates transcription factor NF-kB-mediated protective signaling in primary rat neuronal cultures. J Mol Neurosci. 2005;26(1):27–32.

    CAS  PubMed  Google Scholar 

  8. Roche M, Dufour C, Loonis M, Reist M, Carrupt PA, Dangles O. Olive phenols efficiently inhibit the oxidation of serum albumin-bound linoleic acid and butyrylcholine esterase. Biochim Biophys Acta. 2009;1790(4):240–8.

    CAS  PubMed  Google Scholar 

  9. Taha AY, Cheon Y, Faurot KF, Macintosh B, Majchrzak-Hong SF, Mann JD, et al. Dietary omega-6 fatty acid lowering increases bioavailability of omega-3 polyunsaturated fatty acids in human plasma lipid pools. Prostaglandins Leukot Essent Fatty Acids. 2014;90(5):151–7.

    CAS  PubMed Central  PubMed  Google Scholar 

  10. Kim JJ, Sears DD. TLR4 and insulin resistance. Gastroenterol Res Pract. 2010;2010:S1687–630X.

    Google Scholar 

  11. Saberi M, Woods NB, de Luca C, Schenk S, Lu JC, Bandyopadhyay G, et al. Hematopoietic cell-specific deletion of toll-like receptor 4 ameliorates hepatic and adipose tissue insulin resistance in high-fat-fed mice. Cell Metab. 2009;10(5):419–29.

    CAS  PubMed Central  PubMed  Google Scholar 

  12. Wong SW, Kwon MJ, Choi AM, Kim HP, Nakahira K, Hwang DH. Fatty acids modulate toll-like receptor 4 activation through regulation of receptor dimerization and recruitment into lipid rafts in a reactive oxygen species-dependent manner. J Biol Chem. 2009;284(40):27384–92.

    CAS  PubMed Central  PubMed  Google Scholar 

  13. Tobon-Velasco JC, Cuevas E, Torres-Ramos MA. Receptor for AGEs (RAGE) as mediator of NF-kB pathway activation in neuroinflammation and oxidative stress. CNS Neurol Disord Drug Targets. 2014;13(9):1615–26.

    CAS  PubMed  Google Scholar 

  14. Oh DY, Talukdar S, Bae EJ, Imamura T, Morinaga H, Fan W, et al. GPR120 is an omega-3 fatty acid receptor mediating potent anti-inflammatory and insulin-sensitizing effects. Cell. 2010;142(5):687–98.

    CAS  PubMed Central  PubMed  Google Scholar 

  15. Oh DY, Olefsky JM. Omega 3 fatty acids and GPR120. Cell Metab. 2012;15(5):564–5.

    CAS  PubMed Central  PubMed  Google Scholar 

  16. Scapagnini G, Vasto S, Sonya V, Abraham NG, Nader AG, Caruso C, et al. Modulation of Nrf2/ARE pathway by food polyphenols: a nutritional neuroprotective strategy for cognitive and neurodegenerative disorders. Mol Neurobiol. 2011;44(2):192–201.

    CAS  PubMed  Google Scholar 

  17. Rahman I, Biswas SK, Kirkham PA. Regulation of inflammation and redox signaling by dietary polyphenols. Biochem Pharmacol. 2006;72(11):1439–52.

    CAS  PubMed  Google Scholar 

  18. Zhang X, Zhang G, Zhang H, Karin M, Bai H, Cai D. Hypothalamic IKKbeta/NF-kappaB and ER stress link overnutrition to energy imbalance and obesity. Cell. 2008;135(1):61–73.

    CAS  PubMed Central  PubMed  Google Scholar 

  19. Siriwardhana N, Kalupahana NS, Cekanova M, Le Mieux M, Greer B, Moustaid-Moussa N. Modulation of adipose tissue inflammation by bioactive food compounds. J Nutr Biochem. 2013;24(4):613–23.

    CAS  PubMed  Google Scholar 

  20. Sears B, Ricordi C. Role of fatty acids and polyphenols in inflammatory gene transcription and their impact on obesity, metabolic syndrome and diabetes. Eur Rev Med Pharmacol Sci. 2012;16(9):1137–54.

    CAS  PubMed  Google Scholar 

  21. Kim JY, van de Wall E, Laplante M, Azzara A, Trujillo ME, Hofmann SM, et al. Obesity-associated improvements in metabolic profile through expansion of adipose tissue. J Clin Invest. 2007;117(9):2621–37.

    CAS  PubMed Central  PubMed  Google Scholar 

  22. Chung S, Yao H, Caito S, Hwang JW, Arunachalam G, Rahman I. Regulation of SIRT1 in cellular functions: role of polyphenols. Arch Biochem Biophys. 2010;501(1):79–90.

    CAS  PubMed Central  PubMed  Google Scholar 

  23. Joven J, Rull A, Rodriguez-Gallego E, Camps J, Riera-Borrull M, Hernandez-Aguilera A, et al. Multifunctional targets of dietary polyphenols in disease: a case for the chemokine network and energy metabolism. Food Chem Toxicol. 2013;51:267–79.

    CAS  PubMed  Google Scholar 

  24. Buckley CD, Gilroy DW, Serhan CN. Proresolving lipid mediators and mechanisms in the resolution of acute inflammation. Immunity. 2014;40(3):315–27.

    CAS  PubMed Central  PubMed  Google Scholar 

  25. Serhan CN. Pro-resolving lipid mediators are leads for resolution physiology. Nature. 2014;510:92–101.

    CAS  PubMed Central  PubMed  Google Scholar 

  26. Postic C, Girard J. Contribution of de novo fatty acid synthesis to hepatic steatosis and insulin resistance: lessons from genetically engineered mice. J Clin Invest. 2008;118(3):829–38.

    CAS  PubMed Central  PubMed  Google Scholar 

  27. Perrini S, Ficarella R, Picardi E, Cignarelli A, Barbaro M, Nigro P, et al. Differences in gene expression and cytokine release profiles highlight the heterogeneity of distinct subsets of adipose tissue-derived stem cells in the subcutaneous and visceral adipose tissue in humans. PLoS One. 2013;8(3):e57892.

    CAS  PubMed Central  PubMed  Google Scholar 

  28. Wildman RP, Muntner P, Reynolds K, McGinn AP, Rajpathak S, Wylie-Rosett J, et al. The obese without cardiometabolic risk factor clustering and the normal weight with cardiometabolic risk factor clustering: prevalence and correlates of 2 phenotypes among the US population (NHANES 1999-2004). Arch Intern Med. 2008;168(15):1617–24.

    PubMed  Google Scholar 

  29. Lionetti L, Mollica MP, Lombardi A, Cavaliere G, Gifuni G, Barletta A. From chronic overnutrition to insulin resistance: the role of fat-storing capacity and inflammation. Nutr Metab Cardiovasc Dis. 2009;19(2):146–52.

    CAS  PubMed  Google Scholar 

  30. He Q, Gao Z, Yin J, Zhang J, Yun Z, Ye J. Regulation of HIF-1(alpha) activity in adipose tissue by obesity-associated factors: adipogenesis, insulin, and hypoxia. Am J Physiol Endocrinol Metab. 2011;300(5):E877–85.

    CAS  PubMed Central  PubMed  Google Scholar 

  31. Hotamisligil GS. Inflammation and metabolic disorders. Nature. 2006;444(7121):860–7.

    CAS  PubMed  Google Scholar 

  32. Jaworski K, Sarkadi-Nagy E, Duncan RE, Ahmadian M, Sul HS. Regulation of triglyceride metabolism. IV. Hormonal regulation of lipolysis in adipose tissue. Am J Physiol Gastrointest Liver Physiol. 2007;293(1):G1–4.

    CAS  PubMed Central  PubMed  Google Scholar 

  33. Hotamisligil GS, Murray DL, Choy LN, Spiegelman BM. Tumor necrosis factor alpha inhibits signaling from the insulin receptor. Proc Natl Acad Sci U S A. 1994;91(11):4854–8.

    CAS  PubMed Central  PubMed  Google Scholar 

  34. Weisberg SP, McCann D, Desai M, Rosenbaum M, Leibel RL, Ferrante AW. Obesity is associated with macrophage accumulation in adipose tissue. J Clin Invest. 2003;112(12):1796–808.

    CAS  PubMed Central  PubMed  Google Scholar 

  35. Rosen ED, Sarraf P, Troy AE, Bradwin G, Moore K, Milstone DS, et al. PPAR gamma is required for the differentiation of adipose tissue in vivo and in vitro. Mol Cell. 1999;4(4):611–7.

    CAS  PubMed  Google Scholar 

  36. Ye J. Regulation of PPARgamma function by TNF-alpha. Biochem Biophys Res Commun. 2008;374(3):405–8.

    CAS  PubMed Central  PubMed  Google Scholar 

  37. Scazzocchio B, Vari R, Filesi C, D’Archivio M, Santangelo C, Giovannini C, et al. Cyanidin-3-O-(sup)-glucoside and protocatechuic acid exert insulin-like effects by upregulating PPAR(sup) activity in human omental adipocytes. Diabetes. 2011;60(9):2234–44.

    CAS  PubMed Central  PubMed  Google Scholar 

  38. Cinti S, Mitchell G, Barbatelli G, Murano I, Ceresi E, Faloia E, et al. Adipocyte death defines macrophage localization and function in adipose tissue of obese mice and humans. J Lipid Res. 2005;46(11):2347–55.

    CAS  PubMed  Google Scholar 

  39. Kraemer FB, Takeda D, Natu V, Sztalryd C. Insulin regulates lipoprotein lipase activity in rat adipose cells via wortmannin- and rapamycin-sensitive pathways. Metabolism. 1998;47(5):555–9.

    CAS  PubMed  Google Scholar 

  40. Chabowski A, Coort SL, Calles-Escandon J, Tandon NN, Glatz JF, Luiken JJ, et al. Insulin stimulates fatty acid transport by regulating expression of FAT/CD36 but not FABPpm. Am J Physiol Endocrinol Metab. 2004;287(4):E781–9.

    CAS  PubMed  Google Scholar 

  41. Ozcan U, Cao Q, Yilmaz E, Lee AH, Iwakoshi NN, Ozdelen E, et al. Endoplasmic reticulum stress links obesity, insulin action, and type 2 diabetes. Science. 2004;306(5695):457–61.

    PubMed  Google Scholar 

  42. Horowitz JF, Klein S. Whole body and abdominal lipolytic sensitivity to epinephrine is suppressed in upper body obese women. Am J Physiol Endocrinol Metab. 2000;278(6):E1144–52.

    CAS  PubMed  Google Scholar 

  43. Summers SA. Ceramides in insulin resistance and lipotoxicity. Prog Lipid Res. 2006;45(1):42–72.

    CAS  PubMed  Google Scholar 

  44. Lee BC, Lee J. Cellular and molecular players in adipose tissue inflammation in the development of obesity-induced insulin resistance. Biochim Biophys Acta. 2014;1842(3):446–62.

    CAS  PubMed Central  PubMed  Google Scholar 

  45. Unger RH. Weapons of lean body mass destruction: the role of ectopic lipids in the metabolic syndrome. Endocrinology. 2003;144(12):5159–65.

    CAS  PubMed  Google Scholar 

  46. Thaler JP, Yi CX, Schur EA, Guyenet SJ, Hwang BH, Dietrich MO, et al. Obesity is associated with hypothalamic injury in rodents and humans. J Clin Invest. 2012;122(1):153–62.

    CAS  PubMed Central  PubMed  Google Scholar 

  47. Thaler JP, Schwartz MW. Inflammation and obesity pathogenesis: the hypothalamus heats up. Endocrinology. 2010;151(9):4109–15.

    CAS  PubMed Central  PubMed  Google Scholar 

  48. Yue JT, Lam TK. Lipid sensing and insulin resistance in the brain. Cell Metab. 2012;15(5):646–55.

    CAS  PubMed  Google Scholar 

  49. Milanski M, Degasperi G, Coope A, Morari J, Denis R, Cintra DE, et al. Saturated fatty acids produce an inflammatory response predominantly through the activation of TLR4 signaling in hypothalamus: implications for the pathogenesis of obesity. J Neurosci. 2009;29(2):359–70.

    CAS  PubMed  Google Scholar 

  50. Cintra DE, Ropelle ER, Moraes JC, Pauli JR, Morari J, Souza CT, et al. Unsaturated fatty acids revert diet-induced hypothalamic inflammation in obesity. PLoS One. 2012;7(1):e30571.

    CAS  PubMed Central  PubMed  Google Scholar 

  51. Obici S, Feng Z, Morgan K, Stein D, Karkanias G, Rossetti L. Central administration of oleic acid inhibits glucose production and food intake. Diabetes. 2002;51(2):271–5.

    CAS  PubMed  Google Scholar 

  52. Milanski M, Arruda AP, Coope A, Ignacio-Souza LM, Nunez CE, Roman EA, et al. Inhibition of hypothalamic inflammation reverses diet-induced insulin resistance in the liver. Diabetes. 2012;61(6):1455–62.

    CAS  PubMed Central  PubMed  Google Scholar 

  53. De Souza CT, Araujo EP, Bordin S, Ashimine R, Zollner RL, Boschero AC, et al. Consumption of a fat-rich diet activates a proinflammatory response and induces insulin resistance in the hypothalamus. Endocrinology. 2005;146(1):4192–9.

    PubMed  Google Scholar 

  54. Tripathi YB, Pandey V. Obesity and endoplasmic reticulum (ER) stresses. Front Immunol. 2012;3:240.

    PubMed Central  PubMed  Google Scholar 

  55. Thaler JP, Guyenet SJ, Dorfman MD, Wisse BE, Schwartz MW. Hypothalamic inflammation: marker or mechanism of obesity pathogenesis? Diabetes. 2013;62(8):2629–34.

    CAS  PubMed Central  PubMed  Google Scholar 

  56. Moraes JC, Coope A, Morari J, Cintra DE, Roman EA, Pauli JR, et al. High-fat diet induces apoptosis of hypothalamic neurons. PLoS One. 2009;4(4):e5045.

    PubMed Central  PubMed  Google Scholar 

  57. Borg ML, Omran SF, Weir J, Meikle PJ, Watt MJ. Consumption of a high-fat diet, but not regular endurance exercise training, regulates hypothalamic lipid accumulation in mice. J Physiol. 2012;590(Pt 17):4377–89.

    CAS  PubMed Central  PubMed  Google Scholar 

  58. Auvinen HE, Romijn JA, Biermasz NR, Pijl H, Havekes LM, Smit JW, et al. The effects of high fat diet on the basal activity of the hypothalamus-pituitary-adrenal axis in mice. J Endocrinol. 2012;214(2):191–7.

    CAS  PubMed  Google Scholar 

  59. Serrano A, Pavon FJ, Tovar S, Casanueva F, Senaris R, Dieguez C, et al. Oleoylethanolamide: effects on hypothalamic transmitters and gut peptides regulating food intake. Neuropharmacology. 2011;60(4):593–601.

    CAS  PubMed  Google Scholar 

  60. Chaudhri OB, Field BC, Bloom SR. Gastrointestinal satiety signals. Int J Obes. 2008;32 Suppl 7:S28–31.

    CAS  Google Scholar 

  61. Morinigo R, Moize V, Musri M, Lacy AM, Navarro S, Marin JL, et al. Glucagon-like peptide-1, peptide YY, hunger, and satiety after gastric bypass surgery in morbidly obese subjects. J Clin Endocrinol Metab. 2006;91(5):1735–40.

    CAS  PubMed  Google Scholar 

  62. Markovic TP, Jenkins AB, Campbell LV, Furler SM, Kraegen EW, Chisholm DJ. The determinants of glycemic responses to diet restriction and weight loss in obesity and NIDDM. Diabetes Care. 1998;21(5):687–94.

    CAS  PubMed  Google Scholar 

  63. Pagano G, Cavallo-Perin P, Cassader M, Bruno A, Ozzello A, Masciola Dall’omo AM, et al. An in vivo and in vitro study of the mechanism of prednisone-induced insulin resistance in healthy subjects. J Clin Invest. 1983;72(5):1814–20.

    CAS  PubMed Central  PubMed  Google Scholar 

  64. Donga E, van Dijk M, van Dijk JG, Biermasz NR, Lammers GJ, van Kralingen KW, et al. A single night of partial sleep deprivation induces insulin resistance in multiple metabolic pathways in healthy subjects. J Clin Endocrinol Metab. 2010;95(6):2963–8.

    CAS  PubMed  Google Scholar 

  65. Dali-Youcef N, Mecili M, Ricci R, Andres E. Metabolic inflammation: connecting obesity and insulin resistance. Ann Med. 2013;45(3):242–53.

    CAS  PubMed  Google Scholar 

  66. Uysal KT, Wiesbrock SM, Marino MW, Hotamisligil GS. Protection from obesity-induced insulin resistance in mice lacking TNF-alpha function. Nature. 1997;389:610–4.

    CAS  PubMed  Google Scholar 

  67. Cai D, Yuan M, Frantz DF, Melendez PA, Hansen L, Lee J, et al. Local and systemic insulin resistance resulting from hepatic activation of IKK-beta and NF-kappaB. Nat Med. 2005;11(2):183–90.

    CAS  PubMed Central  PubMed  Google Scholar 

  68. Ebstein W. Zur therapie des diabetes mellitus, insbesordere uber die anwendung des salicylsuaren natron bei demselben. Berliner Klinische Wochenschrift. 1876;13:337–40.

    Google Scholar 

  69. Hecht A, Goldner MF. Reappraisal of the hypoglycemic action of acetylsalicylate. Metabolism. 1959;8:418–28.

    CAS  PubMed  Google Scholar 

  70. Hundal RS, Petersen KF, Mayerson AB, Randhawa PS, Inzucchi S, Shoelson SE, et al. Mechanism by which high-dose aspirin improves glucose metabolism in type 2 diabetes. J Clin Invest. 2002;109(10):1321–6.

    CAS  PubMed Central  PubMed  Google Scholar 

  71. Glass CK, Olefsky JM. Inflammation and lipid signaling in the etiology of insulin resistance. Cell Metabol. 2012;15(5):635–44.

    CAS  Google Scholar 

  72. Samuel VT, Shulman GI. Mechanisms for insulin resistance: common threads and missing links. Cell. 2012;148(5):852–71.

    CAS  PubMed Central  PubMed  Google Scholar 

  73. Tolman KG, Fonseca V, Dalpiaz A, Tan MH. Spectrum of liver disease in type 2 diabetes and management of patients with diabetes and liver disease. Diabetes Care. 2007;30(3):734–43.

    CAS  PubMed  Google Scholar 

  74. Perry RJ, Samuel VT, Petersen KF, Shulman GI. The role of hepatic lipids in hepatic insulin resistance and type 2 diabetes. Nature. 2014;510(7503):84–91.

    CAS  PubMed Central  PubMed  Google Scholar 

  75. German J, Kim F, Schwartz GJ, Havel PJ, Rhodes CJ, Schwartz MW, et al. Hypothalamic leptin signaling regulates hepatic insulin sensitivity via a neurocircuit involving the vagus nerve. Endocrinology. 2009;150(10):4502–11.

    CAS  PubMed Central  PubMed  Google Scholar 

  76. Kraegen EW, Clark PW, Jenkins AB, Daley EA, Chisholm DJ, Storlien LH. Development of muscle insulin resistance after liver insulin resistance in high-fat-fed rats. Diabetes. 1991;40(11):1397–403.

    CAS  PubMed  Google Scholar 

  77. Owyang C, Logsdon CD. New insights into neurohormonal regulation of pancreatic secretion. Gastroenterology. 2004;127(3):957–69.

    CAS  PubMed  Google Scholar 

  78. D’Alessio D. Intestinal hormones and regulation of satiety: the case for CCK, GLP-1, PYY, and Apo A-IV. JPEN J Parenter Enteral Nutr. 2008;32(5):567–8.

    PubMed  Google Scholar 

  79. De Fronzo RA. Dysfunctional fat cells, lipotoxicity and type 2 diabetes. Int J Clin Pract Suppl. 2004;143:9–21.

    Google Scholar 

  80. Diraison F, Yankah V, Letexier D, Dusserre E, Jones P, Beylot M. Differences in the regulation of adipose tissue and liver lipogenesis by carbohydrates in humans. J Lipid Res. 2003;44(4):846–53.

    CAS  PubMed  Google Scholar 

  81. Fabbrini E, Magkos F, Mohammed BS, Pietka T, Abumrad NA, Patterson BW, et al. Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity. Proc Natl Acad Sci U S A. 2009;106(36):15430–5.

    CAS  PubMed Central  PubMed  Google Scholar 

  82. Azuma K, Kadowaki T, Cetinel C, Kadota A, El-Saed A, Kadowaki S, et al. Higher liver fat content among Japanese in Japan compared with non-Hispanic whites in the United States. Metabolism. 2009;58(8):1200–7.

    CAS  PubMed Central  PubMed  Google Scholar 

  83. McLaughlin T, Reaven G, Abbasi F, Lamendola C, Saad M, Waters D, et al. Is there a simple way to identify insulin-resistant individuals at increased risk of cardiovascular disease? Am J Cardiol. 2005;96(3):399–404.

    CAS  PubMed  Google Scholar 

  84. Shoelson SE, Lee J, Goldfine AB. Inflammation and insulin resistance. J Clin Invest. 2006;116(7):1793–801.

    CAS  PubMed Central  PubMed  Google Scholar 

  85. Pang S, Tang H, Zhuo S, Zang YQ, Le Y. Regulation of fasting fuel metabolism by toll-like receptor 4. Diabetes. 2010;59(12):3041–8.

    CAS  PubMed Central  PubMed  Google Scholar 

  86. Straczkowski M, Kowalska I, Nikolajuk A, Dzienis-Straczkowska S, Kinalska I, Baranowski M, et al. Relationship between insulin sensitivity and sphingomyelin signaling pathway in human skeletal muscle. Diabetes. 2004;53(5):1215–21.

    CAS  PubMed  Google Scholar 

  87. Adams JM, Pratipanawatr T, Berria R, Wang E, De Fronzo RA, Sullards MC, et al. Ceramide content is increased in skeletal muscle from obese insulin-resistant humans. Diabetes. 2004;53(1):25–31.

    CAS  PubMed  Google Scholar 

  88. Wei D, Li J, Shen M, Jia W, Chen N, Chen T, Su D, et al. Cellular production of n-3 PUFAs and reduction of n-6-to-n-3 ratios in the pancreatic beta-cells and islets enhance insulin secretion and confer protection against cytokine-induced cell death. Diabetes. 2010;59(2):471–8.

    CAS  PubMed Central  PubMed  Google Scholar 

  89. Duca FA, Yue JT. Fatty acid sensing an the gut and the hypothalamus. Mol Cell Endocrinol. 2014;397:23–33.

    CAS  PubMed  Google Scholar 

  90. Schwartz GJ, Fu J, Astarita G, Li X, Gaetani S, Campolongo P, et al. The lipid messenger OEA links dietary fat intake to satiety. Cell Metab. 2008;8(4):281–8.

    CAS  PubMed Central  PubMed  Google Scholar 

  91. Martinez de Ubago M, Garcia-Oya I, Perez-Perez A, Canfran-Duque A, Quintana-Portillo R, Rodriguez de Fonseca F, et al. Oleoylethanolamide, a natural ligand for PPAR-alpha, inhibits insulin receptor signalling in HTC rat hepatoma cells. Biochim Biophys Acta. 2009;1791(8):740–5.

    CAS  PubMed  Google Scholar 

  92. Field BC, Chaudhri OB, Bloom SR. Bowels control brain: gut hormones and obesity. Nat Rev Endocrinol. 2010;6(8):444–53.

    CAS  PubMed  Google Scholar 

  93. Arruda AP, Milanski M, Coope A, Torsoni AS, Ropelle E, Carvalho DP, et al. Low-grade hypothalamic inflammation leads to defective thermogenesis, insulin resistance, and impaired insulin secretion. Endocrinology. 2011;152(4):1314–26.

    CAS  PubMed  Google Scholar 

  94. Cheung GW, Kokorovic A, Lam CK, Chari M, Lam TK. Intestinal cholecystokinin controls glucose production through a neuronal network. Cell Metab. 2009;10(2):99–109.

    CAS  PubMed  Google Scholar 

  95. le Roux CW, Batterham RL, Aylwin SJ, Patterson M, Borg CM, Wynne KJ, et al. Attenuated peptide YY release in obese subjects is associated with reduced satiety. Endocrinology. 2006;147(1):3–8.

    PubMed  Google Scholar 

  96. Boey D, Lin S, Enriquez RF, Lee NJ, Slack K, Couzens M, et al. PYY transgenic mice are protected against diet-induced and genetic obesity. Neuropeptides. 2008;42(1):19–30.

    CAS  PubMed  Google Scholar 

  97. Ley RE, Turnbaugh PJ, Klein S, Gordon JI. Microbial ecology: human gut microbes associated with obesity. Nature. 2006;444:1022–3.

    CAS  PubMed  Google Scholar 

  98. Shen J, Obin MS, Zhao L. The gut microbiota, obesity and insulin resistance. Mol Aspects Med. 2013;34(1):39–58.

    CAS  PubMed  Google Scholar 

  99. Ding S, Chi MM, Scull BP, Rigby R, Schwerbrock NM, Magness S, et al. High-fat diet: bacterial interactions promote intestinal inflammation which precedes and correlates with obesity and insulin resistance in mouse. PLoS One. 2010;5(8):e12191.

    PubMed Central  PubMed  Google Scholar 

  100. Pendyala S, Walker JM, Holt PR. A high-fat diet is associated with endotoxemia that originates from the gut. Gastroenterology. 2012;142(5):1100–1101.e2.

    CAS  PubMed Central  PubMed  Google Scholar 

  101. Ghanim H, Abuaysheh S, Sia CL, Korzeniewski K, Chaudhuri A, Fernandez-Real JM, et al. Increase in plasma endotoxin concentrations and the expression of Toll-like receptors and suppressor of cytokine signaling-3 in mononuclear cells after a high-fat, high-carbohydrate meal: implications for insulin resistance. Diabetes Care. 2009;32(12):2281–7.

    CAS  PubMed Central  PubMed  Google Scholar 

  102. Laugerette F, Furet JP, Debard C, Daira P, Loizon E, Geloen A, et al. Oil composition of high-fat diet affects metabolic inflammation differently in connection with endotoxin receptors in mice. Am J Physiol Endocrinol Metab. 2012;302(3):E374–86.

    CAS  PubMed  Google Scholar 

  103. Ghoshal S, Witta J, Zhong J, de Villiers W, Eckhardt E. Chylomicrons promote intestinal absorption of lipopolysaccharides. J Lipid Res. 2009;50(1):90–7.

    CAS  PubMed  Google Scholar 

  104. Ford ES, Giles WH, Dietz WH. Prevalence of the metabolic syndrome among US adults: findings from the third National Health and Nutrition Examination Survey. JAMA. 2002;287(3):356–9.

    PubMed  Google Scholar 

  105. Galassi A, Reynolds K, He J. Metabolic syndrome and risk of cardiovascular disease: a meta-analysis. Am J Med. 2006;119(10):812–9.

    CAS  PubMed  Google Scholar 

  106. Yajnik CS. Fetal programming of diabetes: still so much to learn! Diabetes Care. 2010;33(5):1146–8.

    PubMed Central  PubMed  Google Scholar 

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Authors and Affiliations

  1. Inflammation Research Foundation, Marblehead, MA, USA

    Barry Sears PhD

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  1. Barry Sears PhD
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Correspondence to Barry Sears PhD .

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  1. Woman, Mother and Neonate Department, University of Milan, Buzzi Children's Hospital, Milan, Italy

    Enrico Ferrazzi

  2. Inflammation Research Foundation, Marblehead, Massachusetts, USA

    Barry Sears

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© 2015 Springer International Publishing Switzerland

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Sears, B. (2015). The Role of Diet in Inflammation and Metabolic Syndrome. In: Ferrazzi, E., Sears, B. (eds) Metabolic Syndrome and Complications of Pregnancy. Springer, Cham. https://doi.org/10.1007/978-3-319-16853-1_1

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  • DOI: https://doi.org/10.1007/978-3-319-16853-1_1

  • Publisher Name: Springer, Cham

  • Print ISBN: 978-3-319-16852-4

  • Online ISBN: 978-3-319-16853-1

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