Reviev Article. carbohydrate disorders among. wodanowej i lipidowej u kobiet. hormonal and pathophysiological aspects. Zdr Publ 2010;120(4):

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1 Zdr Publ 2010;120(4): Reviev Article wodanowej i lipidowej u kobiet carbohydrate disorders among hormonal and pathophysiological aspects Streszczenie - - tabolicznymi i hormonalnymi charakterystycznymi dla tego substancje takie jak: leptyna, adiponektyna, rezystyna, wistafyna, omentyna, adipsyna, PAI-1, czynnik martwicy nowo w okresie perimenopauzy. Abstract Perimenopause is a transitional period lasting approxi- other words, it is transition between reproductive age and menopause. It is the period directly before menopause when - pause. Diseases which may appear during perimenopause are caused by metabolic and hormonal disturbances characteristic for this period. They are: hypertension, lipid and carbohydrate disorders, osteoporosis. The results of last studies give new insight into the role of the adipose tissue. This tissue is the highly hormonally active gland of internal secretion producing a number of biologically active peptides which can have local as well as systemic effects. Main cells adipose are adipocytes which secrete bioactive substances such as: leptin, adiponectin, resistin, visfatin, omentin, adipsin, PAI-1, TNF-alfa, angiotensinogen, interleukin 6, lipoprotein lipase. Abdominal fat and adipose tissue increase are responsible for the development of insulin resistance. There are hormonal mechanisms regulating correlations between adipose and bone tissue. Osteoblasts show expression of receptors for ghrelin, which stimulates their proliferation and differentiation. Effects of ghrelin on bones are not known yet. It was stated that nocturnal ghrelin concentration correlates with BMD (bone mineral density) among women. The article describes the hormonal and pathophysiological aspects of disorders (hypertension, lipid and carbohydrate disorders, osteoporosis), which appear among women in perimenopause. perimenopauza, zaburzenia gospodarki perimenopause, arterial hypertension, lipid and carbohydrate disorders, abdominal obesity, osteoporosis. 1 Hematology Department, Institute of Hematology and Transfusiology, Warsaw, Poland 2 Physiology Department of Medical University, Lublin, Poland

Abstract Perimenopause is a transitional period lasting approxi- other words, it is transition between reproductive age and menopause. It is the period directly before menopause when - pause.

2 Zdr Publ 2010;120(4) 427 w 2001 roku przez STRAW (Stages of Reproductive Aging najmniej przez 60 dni. Zwykle dotyczy to kobiet w 45 do od rasy [6,8,9]. poty nocne zaburzenia rytmu snu serca zaburzenia libido natomiast wydzielanie inhibiny jajnikowej przez komórki - lutealnej. Cykl ulega skróceniu do dni, ale nadal dzi do dalszego wzrostu poziomu FSH, co powoduje z tym brak inhibin jajnikowych po menopauzie nie jest progesteronem i w konsekwencji do przerostu endometrium. - W okresie perimenopauzy jak i samej menopauzy - [15,18,25-27]. Wieloletnia obserwacja Framingham Heart

poty nocne zaburzenia rytmu snu serca zaburzenia libido - - - natomiast wydzielanie inhibiny jajnikowej przez komórki - lutealnej.

3 428 Zdr Publ 2010;120(4) jak: [25,28-33] leptyna, adiponektyna, rezystyna, wisfatyna, omentyna, adipsyna, PAI-1, czynnik martwicy nowotworów insuliny, glukagonu, tyreotropiny (TSH), hormonu wzrostu, gastryny/cholecystokininy-b, peptydu glukagonopodobnego (GLP-1), receptory typu 1 i 2 dla angiotensyny II (AT 1 i hormonów tarczycy, androgenów, estrogenów, progesteronu, [23,25,29,30,34]. dowe Towarzystwo Diabetologiczne (IDF) w 2005 roku adiponektyna, hormon polipeptydowy, który w swojej budowie posiada sekwencje homologiczne do kolagenu VIII [47] i amyliny [48,49]. Insulina jest jednym z najbardziej jak i dla insulinopodobnego czynnika wzrostu 1 (IGF-1, insulin-like growth factor). przemiany androstendionu w estron. Na podstawie wielu [19,50,51] z BMD. Niedobór estrogenów nasila resorpcje utraty wapnia, co w konsekwencji prowadzi do wzglednej / rozwoju choroby niedokrwiennej serca [7,12,19,53-55]. komórkowej i przestrzeni pozakomórkowej. W komórkach i wody w kanalikach nerkowych [19,24,26,53]. U kobiet

dowe Towarzystwo Diabetologiczne (IDF) w 2005 roku adiponektyna, hormon polipeptydowy, który w swojej budowie posiada sekwencje homologiczne do kolagenu VIII [47] i amyliny [48,49].

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5 430 Zdr Publ 2010;120(4) 38. Jarrett RJ. The metabolic syndrome. Lancet 2005;366: Delhanty PJD, Eerden BCJ, Velde M. Ghrelin and unacylated ghrelin stimulate human ostaoblast growth via mitogen-activated protein kinase pathways in the absence of GHS-R1a. J Endocrinol 2006; 188: Maccarinelli G, Sibilia V, Torsello A. Ghrelin regulates proliferation and differentiation of osteoblastic cells. J Endocrinol 2005; 184: Weiss LA, Langenberg C, Barrett-Conor E. Ghrelin and bone:is there an Res 2006; 21: Features of the metabolic syndrome and risk of non-vertebral fractures: the Tromso study. Osteoporos Int 2006; 17: Joakimsen RM, FonneboV, Magnus JH, Tollan A, Johanne Sogaard A. The Tromso Study: body height, body mass index and fractures. Osteoporosis Int 2005; 16: : Reid I.R. Relationship between fat and bone. Osteoporosis Int 2008; 19: Grey AB, Naot D, Buchanan CM, Cooper GJ, Reid IR. Preptin, another peptide product of the pancreatic beta-cell, is osteogenic in vitro and in vivo. Am J Physiol Endocrinol Metab 2007; 292(1):E osteoblast proliferation and increases mineralized bone volume in adult mice. Biochem Biophys Res Commun 1995; 2007: Horcajada-Molteni MN, Chanteranne B, Lebecque P, Davicco MJ, Coxam V, Young A, Barlet JP. Amylin and bone metabolism in streptozocin-induced diabetic rats. J Bone Miner Res 2001; 16: Rosen CJ, Bouxsein ML. Mechanisms of disease: is osteoporosis the 51. Zhao LJ, Jiang H, Papasian CJ, Maulik D, Drees B, Hamilton J, Deng HW. Correlation of obesity and ostaoporosis:effect of fat mass on the determination of osteoporosis. J Bone Miner Res 2008; 23: Sulak PJ. The perimenopause:a critical time in woman s life. Int J Fertil 1996; 41: DANBERT; Aucott L, Pooblan A, Smith WC, Avenell A, Jung R, Broom J. Effects of weight loss in overweight/obese individuals and long-term hypertension outcomes: a systemic review. Hypertension 2005; 45: therapy on lipoprotein (a) and lipids in postmenopausal women. Arterioscler Thromb Vasc Biol 1994; 14: FC, Sharma AM. Weight loss and the rennin-angiotensin-aldosterone system. Hypertension : Esler M. The symptomatic system of hypertension. Am J Hypertens 2000; 13: angiotensonogen in adipose tissue. Hypertension 1992; 19: The 7 Report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure. The JNC 7 Report. JAMA 2003;289(19): Dr n. med. Hematologii i Transfuzjologii w Warszawie; dr n. med. MASSALSKA Medyczny w Lublinie. ul. Gandhi 14, Warszawa tel. kom.: ela.madro@interia.pl

$Ghrelin and bone:is there an Res 2006; 21:752-7. 43. Features of the metabolic syndrome and risk of non-vertebral fractures: the Tromso study. Osteoporos Int 2006; 17:426-32. 44.$

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