Abstract
Diabetes and obesity have reached epidemic proportions globally, and they are a major contributor to the development of many pathological processes including hypertension, hyperlipidemia, cardiovascular diseases, and certain types of cancer. Increased consumption of more energy-dense, nutrient-poor diets with high levels of carbohydrates and saturated fats, combined with reduced physical activity, has led to currently observed high rates of diabetes and obesity. A strong relationship exists between diabetes and obesity, with fat tissue playing an important role in diabetes, a disease characterized by hyperglycemia, insulin hyposecretion, and insulin resistance. The resistance manifests primarily as impaired ability of the muscle tissue to take up glucose and of the liver to curb glucose output in response to insulin. Eventually, pancreatic beta cell insufficiency leads to overt diabetes.
Obesity is often accompanied by inflammation and insulin resistance and is a preamble to the development of type 2 diabetes. Studies of the last two decades revealed that insulin resistance is multifactorial and coexists with elevated levels of circulating insulin, fatty acids, and oxidative radicals and with low-level inflammation. The first three factors individually cause insulin resistance when applied to rodents or cell cultures. In addition, recent data have revealed that the plasma concentration of inflammatory mediators, such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), is elevated in the insulin-resistant states of obesity and type 2 diabetes, raising questions about the mechanisms underlying inflammation in these two conditions. It is also intriguing that an increase in inflammatory cytokines or indices predicts the future development of diabetes and obesity. Novel approaches in preventing and managing overweight/obesity and diabetes must be developed in order to stop the invasion of these two twin epidemics.
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References
Al-Razi MZ (1958) Kitab al-hawi fit-tibb. Osmania Oriental Publications, Hyderabad
Barnett R (2005) Obesity. Lancet 365:1843
Saad B, Azaizeh H, Said O (2008) Arab herbal medicine. Bot Med Clin Pract 4:31–39
Atkinson RL (2014) Current status of the field of obesity. Trends Endocrinol Metab 25:283–284
Nowicki EM, Billington CJ, Levine AS, Hoover H, Must A et al (2003) Overweight, obesity, and associated disease burden in the veterans affairs ambulatory care population. Mil Med 168:252–256
Padwal R, Li SK, Lau DC (2003) Long-term pharmacotherapy for overweight and obesity: a systematic review and meta-analysis of randomized controlled trials. Int J Obes Relat Metab Disord 27:1437–1446
Saad B, Zaid H, Said O (2013) Tradition and perspectives of diabetes treatment in Greco-Arab and Islamic medicine. In: Watson RR, Preedy VR (eds) Bioactive food as dietary interventions for diabetes. Academic Press, San Diego, pp 319–326
Zaid H, Saad B (2013) State of the art of diabetes treatment in Greco-Arab and Islamic medicine. In: Watson RR, Preedy VR (eds) Bioactive food as dietary interventions for diabetes. Academic Press, San Diego/London, pp 327–335
“Annual Report 2014” (PDF). IDF. International Diabetes Federation. Retrieved 13 July 2016
Yuen L, Wong VW (2015) Gestational diabetes mellitus: challenges for different ethnic groups. World J Diabetes 6:1024–1032
Santangelo C, Zicari A, Mandosi E, Scazzocchio B, Mari E et al (2016) Could gestational diabetes mellitus be managed through dietary bioactive compounds? Current knowledge and future perspectives. Br J Nutr 115:1129–1144
Soltesz G, Patterson CC, Dahlquist G (2007) Worldwide childhood type 1 diabetes incidence–what can we learn from epidemiology? Pediatr Diabetes 8 Suppl 6:6–14
Krzewska A, Ben-Skowronek I (2016) Effect of associated autoimmune diseases on type 1 diabetes mellitus incidence and metabolic control in children and adolescents. Biomed Res Int 2016:6219730
Serena G, Camhi S, Sturgeon C, Yan S, Fasano A (2015) The role of gluten in celiac disease and type 1 diabetes. Nutrients 7:7143–7162
Butalia S, Kaplan GG, Khokhar B, Rabi DM (2016) Environmental risk factors and type 1 diabetes: past, present, and future. Can J Diabetes 40(6):586–593
Bluestone JA, Herold K, Eisenbarth G (2010) Genetics, pathogenesis and clinical interventions in type 1 diabetes. Nature 464:1293–1300
de Beeck AO, Eizirik DL (2016) Viral infections in type 1 diabetes mellitus–why the beta cells? Nat Rev Endocrinol 12:263–273
Unger RH (1991) Diabetic hyperglycemia: link to impaired glucose transport in pancreatic beta cells. Science 251:1200–1205
Zaid H, Antonescu CN, Randhawa VK, Klip A (2008) Insulin action on glucose transporters through molecular switches, tracks and tethers. Biochem J 413:201–215
Hawley JA (2004) Exercise as a therapeutic intervention for the prevention and treatment of insulin resistance. Diabetes Metab Res Rev 20:383–393
Kaneto H, Obata A, Kimura T, Shimoda M, Okauchi S et al (2016) Beneficial effects of SGLT2 inhibitors for preservation of pancreatic beta-cell function and reduction of insulin resistance. J Diabetes 9(3):219–225
Lee JO, Lee SK, Jung JH, Kim JH, You GY et al (2011) Metformin induces Rab4 through AMPK and modulates GLUT4 translocation in skeletal muscle cells. J Cell Physiol 226:974–981
Huang S, Czech MP (2007) The GLUT4 glucose transporter. Cell Metab 5:237–252
Holman GD, Cushman SW (1994) Subcellular localization and trafficking of the GLUT4 glucose transporter isoform in insulin-responsive cells. BioEssays 16:753–759
Hou JC, Pessin JE (2007) Ins (endocytosis) and outs (exocytosis) of GLUT4 trafficking. Curr Opin Cell Biol 19:466–473
Bryant NJ, Govers R, James DE (2002) Regulated transport of the glucose transporter GLUT4. Nat Rev Mol Cell Biol 3:267–277
Zaid H, Talior-Volodarsky I, Antonescu C, Liu Z, Klip A (2009) GAPDH binds GLUT4 reciprocally to hexokinase-II and regulates glucose transport activity. Biochem J 419:475–484
Kahn SE, Hull RL, Utzschneider KM (2006) Mechanisms linking obesity to insulin resistance and type 2 diabetes. Nature 444:840–846
Said O, Fulder S, Khalil K, Azaizeh H, Kassis E et al (2008) Maintaining a physiological blood glucose level with ‘glucolevel’, a combination of four anti-diabetes plants used in the traditional Arab herbal medicine. Evid Based Complement Alternat Med 5:421–428
Khanna P, Jain SC, Panagariya A, Dixit VP (1981) Hypoglycemic activity of polypeptide-p from a plant source. J Nat Prod 44:648–655
Omar EA, Kam A, Alqahtani A, Li KM, Razmovski-Naumovski V et al (2010) Herbal medicines and nutraceuticals for diabetic vascular complications: mechanisms of action and bioactive phytochemicals. Curr Pharm Des 16:3776–3807
Witters LA (2001) The blooming of the French lilac. J Clin Invest 108:1105–1107
Nyenwe EA, Jerkins TW, Umpierrez GE, Kitabchi AE (2011) Management of type 2 diabetes: evolving strategies for the treatment of patients with type 2 diabetes. Metabolism 60:1–23
Baur JA, Pearson KJ, Price NL, Jamieson HA, Lerin C et al (2006) Resveratrol improves health and survival of mice on a high-calorie diet. Nature 444:337–342
Lagouge M, Argmann C, Gerhart-Hines Z, Meziane H, Lerin C et al (2006) Resveratrol improves mitochondrial function and protects against metabolic disease by activating SIRT1 and PGC-1alpha. Cell 127:1109–1122
WHO (2015) Fact sheet: obesity and overweight. Available online at: http://www.who.int/mediacentre/factsheets/fs311/en/
Battles W. Nutrition, physical activity, and obesity. In Centers for Disease Control and Prevention. http://www.cdc.gov/winnablebattles/obesity
WHO (1998) The World Health Report 1998—life in the 21st century: a vision for all. World Health Organization, Geneva
WHO (1998) Obesity: preventing and managing the global epidemic. Report of a WHO consultation on obesity Geneva, 3–5 June 1997 Geneva: World Health Organization, 1998 WHO/NUT/NCD/98.1
Woods SC, Seeley RJ, Porte D Jr, Schwartz MW (1998) Signals that regulate food intake and energy homeostasis. Science 280:1378–1383
Guyenet SJ, Schwartz MW (2012) Clinical review: regulation of food intake, energy balance, and body fat mass: implications for the pathogenesis and treatment of obesity. J Clin Endocrinol Metab 97:745–755
Munyaka PM, Khafipour E, Ghia JE (2014) External influence of early childhood establishment of gut microbiota and subsequent health implications. Front Pediatr 2:109
Baothman OA, Zamzami MA, Taher I, Abubaker J, Abu-Farha M (2016) The role of gut microbiota in the development of obesity and diabetes. Lipids Health Dis 15:108
Cox AJ, West NP, Cripps AW (2015) Obesity, inflammation, and the gut microbiota. Lancet Diabetes Endocrinol 3:207–215
Delzenne NM, Neyrinck AM, Backhed F, Cani PD (2011) Targeting gut microbiota in obesity: effects of prebiotics and probiotics. Nat Rev Endocrinol 7:639–646
Ley RE, Backhed F, Turnbaugh P, Lozupone CA, Knight RD et al (2005) Obesity alters gut microbial ecology. Proc Natl Acad Sci U S A 102:11070–11075
Murphy EF, Cotter PD, Healy S, Marques TM, O'Sullivan O et al (2010) Composition and energy harvesting capacity of the gut microbiota: relationship to diet, obesity and time in mouse models. Gut 59:1635–1642
Turnbaugh PJ, Ley RE, Mahowald MA, Magrini V, Mardis ER et al (2006) An obesity-associated gut microbiome with increased capacity for energy harvest. Nature 444:1027–1031
Liou AP, Paziuk M, Luevano JM Jr, Machineni S, Turnbaugh PJ et al (2013) Conserved shifts in the gut microbiota due to gastric bypass reduce host weight and adiposity. Sci Transl Med 5:178ra141
Gao Z, Yin J, Zhang J, Ward RE, Martin RJ et al (2009) Butyrate improves insulin sensitivity and increases energy expenditure in mice. Diabetes 58:1509–1517
den Besten G, van Eunen K, Groen AK, Venema K, Reijngoud DJ et al (2013) The role of short-chain fatty acids in the interplay between diet, gut microbiota, and host energy metabolism. J Lipid Res 54:2325–2340
Bjursell M, Admyre T, Goransson M, Marley AE, Smith DM et al (2011) Improved glucose control and reduced body fat mass in free fatty acid receptor 2-deficient mice fed a high-fat diet. Am J Physiol Endocrinol Metab 300:E211–E220
Kimura I, Ozawa K, Inoue D, Imamura T, Kimura K et al (2013) The gut microbiota suppresses insulin-mediated fat accumulation via the short-chain fatty acid receptor GPR43. Nat Commun 4:1829
Conterno L, Fava F, Viola R, Tuohy KM (2011) Obesity and the gut microbiota: does up-regulating colonic fermentation protect against obesity and metabolic disease? Genes Nutr 6:241–260
Caesar R, Nygren H, Orešič M, Bäckhed F (2016) Interaction between dietary lipids and gut microbiota regulates hepatic cholesterol metabolism. J Lipid Res 5:474–481
Moreno-Indias I, Cardona F, Tinahones FJ, Queipo-Ortuno MI (2014) Impact of the gut microbiota on the development of obesity and type 2 diabetes mellitus. Front Microbiol 5:190
Harakeh SM, Khan I, Kumosani T, Barbour E, Almasaudi SB et al (2016) Gut microbiota: a contributing factor to obesity. Front Cell Infect Microbiol 6:95
Scott KP, Antoine JM, Midtvedt T, van Hemert S (2015) Manipulating the gut microbiota to maintain health and treat disease. Microb Ecol Health Dis 26:25877
Zhang L, Huang Y, Zhou Y, Buckley T, Wang HH (2013) Antibiotic administration routes significantly influence the levels of antibiotic resistance in gut microbiota. Antimicrob Agents Chemother 57:3659–3666
Burrows MP, Volchkov P, Kobayashi KS, Chervonsky AV (2015) Microbiota regulates type 1 diabetes through Toll-like receptors. Proc Natl Acad Sci U S A 112:9973–9977
Donath MY (2016) Multiple benefits of targeting inflammation in the treatment of type 2 diabetes. Diabetologia 59:679–682
Pillon NJ, Azizi PM, Li YE, Liu J, Wang C et al (2015) Palmitate-induced inflammatory pathways in human adipose microvascular endothelial cells promote monocyte adhesion and impair insulin transcytosis. Am J Physiol Endocrinol Metab 309:E35–E44
Cani PD, Possemiers S, Van de Wiele T, Guiot Y, Everard A et al (2009) Changes in gut microbiota control inflammation in obese mice through a mechanism involving GLP-2-driven improvement of gut permeability. Gut 58:1091–1103
Hamilton MK, Boudry G, Lemay DG, Raybould HE (2015) Changes in intestinal barrier function and gut microbiota in high-fat diet-fed rats are dynamic and region dependent. Am J Physiol Gastrointest Liver Physiol 308:G840–G851
Chadt A, Scherneck S, Joost HG, Al Hasani H (2000) Molecular links between Obesity and Diabetes: “Diabesity”. [Updated 2014 May 1]. In: De Groot LJ, Chrousos G, Dungan K et al (eds) Endotext. MDText.com, Inc., South Dartmouth
Verma S, Hussain ME (2017) Obesity and diabetes: an update. Diabetes Metab Syndr 11(1):73–79
Fink LN, Costford SR, Lee YS, Jensen TE, Bilan PJ et al (2014) Pro-inflammatory macrophages increase in skeletal muscle of high fat-fed mice and correlate with metabolic risk markers in humans. Obesity (Silver Spring) 22:747–757
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Saad, B., Zaid, H., Shanak, S., Kadan, S. (2017). Introduction to Diabetes and Obesity. In: Anti-diabetes and Anti-obesity Medicinal Plants and Phytochemicals. Springer, Cham. https://doi.org/10.1007/978-3-319-54102-0_1
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DOI: https://doi.org/10.1007/978-3-319-54102-0_1
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