Praca Poglądowa Reviev Article

Zdr Publ 2010;120(4):426-430
Reviev Article
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wodanowej i lipidowej u kobiet
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carbohydrate disorders among
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Streszczenie
Abstract
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tabolicznymi i hormonalnymi charakterystycznymi dla tego
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w okresie perimenopauzy.
Perimenopause is a transitional period lasting approxi $ = 7
other words, it is transition between reproductive age and
menopause. It is the period directly before menopause when
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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
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perimenopause, arterial hypertension, lipid and
carbohydrate disorders, abdominal obesity, osteoporosis.
1
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Hematology Department, Institute of Hematology and Transfusiology, Warsaw, Poland
Physiology Department of Medical University, Lublin, Poland
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pt. “Zdrowie Publiczne wyzwaniem XXI wieku”, Lublin,
1. ;“;.#
››;
1996; 23:137-45.
2. 22 /—Š “3/&/$™$
and Infertility. Lipincott Wiliams and Wilkins, Baltimore1999.
3. Speroff L. The perimenopausal transition. Ann NY Acad Sci. 2000;
900:375-92.
4. ; “ ; 9" 8 / .# transition. Am J Hum Biol.1992; 4:37-46.
5. <› 3™ ;“ ; .# ;#
+ž Š# *
an epidemiologic investigation of the menopause. J Am Med Womens
Assoc.1995;50(2):45-9.
6. 9"8 ;“;<›
2222$
age of menopause. J Clin Epidemiology 1989; 42:1031-8.
7. ,.“"
Medycyna po Dyplomie 1997; 6:13-8.
8. Richardson SJ. The biological basis of the menopause. Bailliere’s
Clinical Endocrinology and metabolism. 1993; 7:1-15.
9. 24 $#$2
&#
Dis. 1987; 40:995-1002.
10. 9
 < 9,! 9*!¡
1994
429
11. ;
# “#“. ; &™$
š#
and bone mineral density among community-based postmenopausal
women. Postgrad Am Med J 1992; 68:908-13.
12. —##
#V~~—2+Š!=
Group. WHO, Genewa,1996.
13. Riggs BL, Melton LJ. Involutional osteoporosis. New Engl J Med 1986;
314;1676-87.
14. . ( 7 # /  —X
;Š / ,.+$#
$ = .34X5 ;
^|¡
6:63-7.
15. 9/™$#'"
%
"“
2000; 52:S6-9.
16. Burger HG ,Dudley E ,Manners P, Groome N, Robertson DM. Early
follicular phase serum FSH as a function of age: the roles of inhibin B,
inhibin A and estradiol. Climacteric 2003; 3:17-24.
17. Š$ 8; —"
8; 9# “9 # & #
< .™ 4
"$&8 “#
/ .8 —$+ Givens DH, Waters D. Effects of estrogenreplacement on the progression
of coronary artery atherosclerosis. N Engl J Med 2000; 343:522-9.
18. Hulley S, Grady D, Busk T, Furberg C, Herrington D, Riggs B,
Vittinghoff E. Randomized trial of estrogen plus progestin for secondary
prevention of coronary heart disease in postmenopausal women.
Heart and Estrogen/Progestin Replacement Study Research Group.
JAMA1998; 280:605-13.
19. , . 8$ $ ‹" ¢
Partner 2004; 26:313-22.
20. Hee J, MacNaughton J, Bangah M, Burger HG. Perimenopausal pattern
of gonadotropins, immunoreactive inhibin, oestradiol and progesterone.
Maturitas 1993;18:9-20.
21. “# 9 4  !"  & 7› ^¡
106:473-81.
22. “## ™› ›8 + 9™ ; “
D,Vassan R. Obesity and the risk of heart failure. N Engl J Med 2002;
347:305-12.
23. “— !,9 Š‚.
X
$$^¡6^*~V~X^Y
24. 
<3‚$ $
; “'^_
25. Bellanger TM, Bray GA. Obesity related morbidity and mortality. J La
State Med Soc 2005; 157(1):S42-9.
26. Chiang B, Perlman L, Epstein F. Overweight and hypertension. A
review. Circulation 1996; 39:403-21.
27. Hubert HB, Feinleib M, McNamara PM, Castelli WP. Obesity as an
independent risk factor for cardiovascular disease: a 26-year followup of participants in the Framingham Heart Study. Circulation 1983;
67(5):968-77.
28. &# &“™ 9›‹ & 38 Š9 /<9 9
N, Myers DE, Nicholson GC, Reid IR. Leptin directly regulated bone
cell function in vitro and reduces bone fragility in vivo. J Endocrinol
2002;175:405-15.
29. Hall J. The kidney, hypertension and obesity. Hypertension 2003;
41:625-33.
30. “ X
4•!"™
Metab Clin North Am 2003; 32:895-914.
31. Sharma A. Is there rationale for angiotensin blockade in the management
2"#£Š^|¡||*V^X~
32. .#. /4 “# ;8 9
$
9 —$$9
acts on human marrow stromal cells to enhance differentiation to
osteoblasts and to inhibit differentiation to adipocytes. Endocrinol 1999;
140:1630-8
33. +9 +“ 8
"";!›$#"*› consequences and causes of a growing public health problem. Am J Med
Sci 2006; 331:166-74.
34. Hall J. Pathophysiology of obesity hypertension. Curr Hypertens Rep
2000; 2:139-47.
35. <"“/ ‚ #784™$.4&
/
.#"¥=
2005; 366:1059-62.
36. DeNiro W, Tchernof A, Dionne I, Toth M, Ades P, Sites C, Poehlman E.
Contribution of abdominal adiposity to age-related differences in insulin
sensitivity and plasma lipids in healthy nonobese women. Diabetes
2001; 24(5):925-32.
37. Eckel R, Grundy S, Zimmet P. The metabolic syndrome. Lancet 2005;
365:1415-28
430
38. Jarrett RJ. The metabolic syndrome. Lancet 2005;366:1922.
39. .#784
=2"*#*¦
2$¦"¦¦;"§§=2
40. Delhanty PJD, Eerden BCJ, Velde M. Ghrelin and unacylated ghrelin
stimulate human ostaoblast growth via mitogen-activated protein kinase
pathways in the absence of GHS-R1a. J Endocrinol 2006; 188:37-47.
41. Maccarinelli G, Sibilia V, Torsello A. Ghrelin regulates proliferation and
differentiation of osteoblastic cells. J Endocrinol 2005; 184:249-56.
42. Weiss LA, Langenberg C, Barrett-Conor E. Ghrelin and bone:is there an
£.##9
9;
Res 2006; 21:752-7.
43. <# < # Š 9 /“ 4"¨  —;
Features of the metabolic syndrome and risk of non-vertebral fractures:
the Tromso study. Osteoporos Int 2006; 17:426-32.
44. Joakimsen RM, FonneboV, Magnus JH, Tollan A, Johanne Sogaard
A. The Tromso Study: body height, body mass index and fractures.
Osteoporosis Int 2005; 16:1330-8.
45. 3$
.¨ Š/; “ ™<9 2*$›£<™V~~}¡
147:3-16.
46. Reid I.R. Relationship between fat and bone. Osteoporosis Int 2008;
19:595-606.
47. &#  & “™ 9› ‹ + ; •
•  ; &#¨< Grey AB, Naot D, Buchanan CM, Cooper GJ, Reid IR. Preptin, another
peptide product of the pancreatic beta-cell, is osteogenic in vitro and in
vivo. Am J Physiol Endocrinol Metab 2007; 292(1):E117-22.
48. &#  & “™ & / — 7— < osteoblast proliferation and increases mineralized bone volume in adult
mice. Biochem Biophys Res Commun 1995; 2007:133-9.
49. Horcajada-Molteni MN, Chanteranne B, Lebecque P, Davicco MJ,
Coxam V, Young A, Barlet JP. Amylin and bone metabolism in
streptozocin-induced diabetic rats. J Bone Miner Res 2001; 16:958-65.
50. Rosen CJ, Bouxsein ML. Mechanisms of disease: is osteoporosis the
"2"£3&—#
^6¡^*YX|Y
51. Zhao LJ, Jiang H, Papasian CJ, Maulik D, Drees B, Hamilton J, Deng
HW. Correlation of obesity and ostaoporosis:effect of fat mass on the
determination of osteoporosis. J Bone Miner Res 2008; 23:17-29.
Zdr Publ 2010;120(4)
52. Sulak PJ. The perimenopause:a critical time in woman’s life. Int J Fertil
1996; 41:85-9.
53. ;$=* !( "$ “'*
DANBERT; 2008.
54. 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; 45:1035-41.
55. “& $Š& &#8Š ;©“™222#
therapy on lipoprotein (a) and lipids in postmenopausal women.
Arterioscler Thromb Vasc Biol 1994; 14:275-81.
56. ™$ 9#  / “   #$ 9 ; 
2
FC, Sharma AM. Weight loss and the rennin-angiotensin-aldosterone
system. Hypertension 2005.45:356-62.
57. Esler M. The symptomatic system of hypertension. Am J Hypertens
2000; 13:99-105.
58. 4#— “#9 #;.
X=
$
2
angiotensonogen in adipose tissue. Hypertension 1992; 19:339-44.
59. 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):2560-72.
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