REVIEW PAPER
The influence of adipose tissue and selected adipokines on insulin resistance and development of diabetes mellitus type 2
 
More details
Hide details
1
Klinika Diabetologii Instytut Medycyny Wsi im. Witolda Chodźki w Lublinie
2
II Klinika Chirurgii Ogólnej, Gastroenterologicznej i Nowotworów Układu Pokarmowego Samodzielny Publiczny Szpital Kliniczny nr 1 w Lublinie
3
Klinika Chorób Wewnętrznych Samodzielny Publiczny Szpital Kliniczny Nr 1 w Lublinie
4
Klinika Chorób Wewnętrznych i Nadciśnienia Tętniczego z Pododdziałem Chorób Zawodowych i Szybkiej Diagnostyki Instytut Medycyny Wsi im. Witolda Chodźki w Lublinie
CORRESPONDING AUTHOR
Patrycja Kamila Kozak-Nurczyk   

Klinika Diabetologii Instytut Medycyny Wsi im. Witolda Chodźki w Lublinie, Jaczewskiego 2, 20-090 Lublin, Polska
 
Med Og Nauk Zdr. 2018;24(4):210–213
KEYWORDS
TOPICS
ABSTRACT
Introduction and objective:
Obesity is a predisposing factor for the development of insulin resistance and, as a consequence, diabetes mellitus type 2. The decrease in insulin sensitivity in obesity results from a disorder of glucose homeostasis, causing hyperinsulinaemia and disposal of the pancreatic reserve. These processes can be regulated by various compounds produced by fat cells such as, free fatty acids and adipokines. The aim of the study is to present the influence of adipose tissue and its products on insulin resistance.

Brief description of the state of knowledge:
Fatty tissue can be divided into white and brown. Brown adipose tissue is particularly interesting because of its beneficial effects that may be important in obesity and diabetes protection. It provides postprandial thermogenesis, which allows excess energy to dissipate in the form of heat. Adipose tissue can also be divided in terms of its location as subcutaneous and visceral (VAT). VAT is a very metabolically active tissue. It releases many hormones, cytokines and metabolites. Adipokines are active biological substances produced exclusively by fat cells that combine the functions of hormones and cytokines. They have influence on many physiological processes such as carbohydrate metabolism, inflammation, angiogenesis or atherogenesis. This work focuses on the most important adipokines that may have a potential role in limiting the phenomenon of insulin resistance.

Summary:
Visceral fat tissue has become a promising place for the search of substances and mechanisms used in treatment of metabolic syndrome and type 2 diabetes.

 
REFERENCES (35)
1.
Siemińska L. Tkanka tłuszczowa. Patofizjologia, rozmieszczenie, różnice płciowe oraz znaczenie w procesach zapalnych i nowotworowych. Endokrynol Pol. 2007; 58(4): 330–342.
 
2.
Nedergaard J, Bengtsson T, Cannon B. Unexpected evidence for active brown adipose tissue in adult humans. Am. J. Physiol. Endocrinol. Metab. 2007; 293: E444–E452.
 
3.
Saito M. Brown adipose tissue as a regulator of energy expenditure and body fat in humans. Diabetes Metab. J. 2013; 37: 22–29.
 
4.
Saito M, Okamatsu-Ogura Y, Matsushita M, Watanabe K, Yoneshiro T, Nio-Kobayashi J et. al. High incidence of metabolically active brown adipose tissue in healthy adult humans: effect of cold exposure and adiposity. Diabetes. 2009; 58(7): 1526–1531.
 
5.
Frühbeck G, Gómez-Ambrosi J, Muruzábal JF, Burrell MA. The adipo¬cyte: a model for integration of endocrine and metabolic signaling in energy metabolism regulation. Am J Physiol Endocrinol Metab. 2001; 280: E827–E847.
 
6.
Murawska-Ciałowicz E. Tkanka tłuszczowa – charakterystyka morfologiczna i biochemiczna różnych depozytów. Postepy Hig Med Dosw (Online). 2017; 71: 466–484.
 
8.
Giordano A, Smorlesi A, Frontini A, Barbatelli G, Cinti S. White, brown and pink adipocytes: the extraordinary plasticity of the adipose organ. Eur J Endocrinol. 2014; 170: R159–R171.
 
9.
Himms-Hagen J, Melnyk A, Zingaretti MC, Ceresi E, Barbatelli G, Cinti S. Multilocular fat cells in WAT of CL-316243-treated rats derive directly from white adipocytes. Am J Physiol Cell Physiol. 2000; 279: C670–C681.
 
10.
Smorlesi A, Frontini A, Giordano A, Cinti S: The adipose organ: white¬-brown adipocyte plasticity and metabolic inflammation. Obes Rev. 2012; 13 (Suppl. 2): 83–96.
 
11.
Pouliot MC, Despres JP, Nadeau A, Moorjani S, Prud’Homme D, Lupien PJ et al. Visceral obesity in men. Associations with glucose tolerance, plasma insulin, and lipoprotein levels. Diabetes. 1992; 7: 826–43.
 
12.
Banerji MA, Lebowitz J, Chaiken RL, Gordon D, Kral JG, Lebovitz HE. Relationship of visceral adipose tissue and glucose disposal is independent of sex in black NIDDM subjects. AMJ Physiol. 1997; 273 (2 Pt 1): E425–321.
 
13.
Montague CT, O’Rahilly S. The perils of portliness: cause and conse¬quences of visceral adiposity. Diabetes. 2000; 6: 833–8.
 
14.
Boden G. Role of fatty acids in pathogenesis of insulin resistance and NIDDM. Diabetes. 1997; 1: 3–10.
 
15.
Moller DE, Kaufman KD. Metabolic syndrome: a clinical and molecular perspective. Annu Rev Med. 2005; 56: 45–62.
 
16.
Koerner A, Kratzsch J, Kiess W. Adipocytokines: leptin – the classical, resistin – the controversical, adiponectin – the promising, and more to come. Best Prac Res Clin Endocrinol Metab. 2005; 19(4): 525–546.
 
17.
Kumor A., Maciak I, Kozak-Michałowska I. Leptyna – hormon o wie¬lokierunkowym działaniu. Diag Lab. 2004; 40: 179–190.
 
18.
Meier U, Gressner AM. Endocrine regulation of energy metabolism: Review of pathobiochemical and clinical chemical aspects of leptin, ghrelin, adiponectin and resistin. Clin Chem. 2004; 50(9): 1511–1525.
 
19.
Wabitsch M, Funcke JB, Lennerz B, Kuhnle-Krahl U, Lahr G, Debatin KM et al. Biologically Inactive Leptin and Early-Onset Extreme Obesity. N Engl J Med. 2015; 372(1): 48–54.
 
20.
Pan H, Guo J, Su Z. Advances in understanding the interrelations be¬tween leptin resistance and obesity. Physiol Behav. 2014; 130: 157–169.
 
21.
Abdella NA, Mojiminiyi OA, Moussa MA, Zaki M, Al Mohammedi H, Al Ozairi ES et al. Plasma leptin concentration in patients with Type 2 diabetes: relationship to cardiovascular disease risk factors and insulin resistance. Diabet Med. 2005; 22: 278–285.
 
22.
Wannamethee SG, Tchernova J, Whincup P, Lowe GD, Kelly A, Rumley A et al. Plasma leptin: associations with metabolic, inflammatory and haemostatic risk factors for cardiovascular disease. Atherosclerosis. 2007; 191: 418–426.
 
23.
Seufert J. Leptin Effects on Pancreatic β-Cell Gene Expression and Function. Diabetes. 2004; 53(suppl 1): S152–S158.
 
24.
Cawthorn WP, Scheller EL, Learman BS, Parlee SD, Simon BR, Mori H et al. Bone marrow adipose tissue is an endocrine organ that contributes to increased circulating adiponectin during caloric restriction. Cell Metab. 2014; 20(2): 368–375.
 
25.
Stefan N, Bunt JC, Salbe AD, Funahashi T, Matsuzawa Y, Tataranni PA. Plasma adiponectin concentrations in children: Relationships with obesity and insulinemia. J Clin Endocrinol Metab. 2002; 87: 4652–4656.
 
26.
Fang H, Judd RL. Adiponectin regulation and function. Compr Physiol. 2018; 8(3): 1031–1063.
 
27.
Weyer C, Funahashi T, Tanaka S, Hotta K, Matsuzawa Y, Pratley RE et al. Hypoadiponectinemia in obesity and type 2 diabetes: Close associa¬tion with insulin resistance and hyperinsulinemia. J Clin Endocrinol Metab. 2001; 86: 1930–1935.
 
28.
Revollo JR, Korner A, Mills KF, Satoh A, Wang T, Garten A et al. Nampt/ PBEF/Visfatin regulates insulin secretion in beta cells as a systemic NAD biosynthetic enzyme. Cell Metab. 2007; 6(5): 363–375.
 
29.
Chen MP, Chung FM, Chang DM, Tsai JC, Huang HF, Shin SJ et al. Elevated plasma level of visfatin/pre-B cell colony-enhancing factor in patients with type 2 diabetes mellitus. J Clin Endocrinol Metab. 2006; 91(1): 295–299.
 
30.
Chang HM, Lee HJ, Park HS, Kang JH, Kim KS, Song YS et al. Effects of weight reduction on serum vaspin concentrations in obese subjects: modification by insulin resistance. Obesity (Silver Spring). 2010; 18(11): 2105–2110.
 
31.
Chang HM, Park HS, Park CY, Song YS, Jang YJ. Association between serum vaspin concentrations and visceral adipose tissue in Korean subjects. Metabolism. 2010; 59(9): 1276–1281.
 
32.
Nakatsuka A, Wada J, Iseda I, Teshigawara S, Higashio K, Murakami K et al. Vaspin is an adipokine ameliorating ER stress in obesity as a ligand for cell-surface GRP78/MTJ-1 complex. Diabetes. 2012; 61(11): 2823–2832.
 
33.
Zhang Q, Zhu L, Zheng M, Fan C, Li Y, Zhang D et al. Changes of serum omentin-1 levels in normal subjects, type 2 diabetes and type 2 diabetes with overweight and obesity in Chinese adults. Ann Endocrinol (Paris). 2014; 75: 171–175.
 
34.
Lapointe M, Poirier P, Martin J, Bastien M, Auclair A, Cianflone K. Omentin changes following bariatric surgery and predictive links with biomarkers for risk of cardiovascular disease. Cardiovasc Diabetol. 2014; 13: 124.
 
35.
Yang RZ, Lee MJ, Hu H, Pray J, Wu HB, Hansen BC et al. Identification of omentin as a novel depot-specific adipokine in human adipose tissue: possible role in modulating insulin action. Am J Physiol Endocrinol Metab. 2006; 290: E1253–E1261.
 
eISSN:2084-4905
ISSN:2083-4543