Introducing the thyroid gland as another victim of the insulin resistance syndrome

被引:202
作者
Rezzonico, Jorge [2 ]
Rezzonico, Mariana [2 ]
Pusiol, Eduardo [2 ]
Pitoia, Fabian [1 ]
Niepomniszcze, Hugo [1 ]
机构
[1] Univ Buenos Aires, Div Endocrinol, Hosp Clin, Buenos Aires, DF, Argentina
[2] Ctr Privado Endocrinol, Mendoza, Argentina
关键词
D O I
10.1089/thy.2007.0223
中图分类号
R5 [内科学];
学科分类号
1002 [临床医学]; 100201 [内科学];
摘要
Background: Insulin is a thyroid growth factor that stimulates proliferation of thyroid cells in culture. In order to evaluate the effects of insulin resistance ( IR) on the thyroid gland, we developed a prospective study in euthyroid women. Methods: One hundred eleven women ( mean age 32.2 +/- 7 years) were evaluated by a thyroid ultrasound ( US) and basal and postprandial serum insulin. Subjects were divided into four groups as follows: G1 ( n= 42), subjects with IR and obesity; G2 ( n = 21), subjects with obesity without IR; G3 ( n =17), subjects with IR and normal weight; and G4 ( n =31) control group ( without IR and obesity). Results: The thyroid volume ( TV), measured by US, showed the following values: G1, 17 +/- 3mL; G2, 13.8 +/- 2.8 mL; G3, 16.2 +/- 2.1mL; and G4,12.1 +/- 2.4 mL. There was no significant difference in TV between G1 and G3, but differences between G1 and G2, and between G3 and G4 were significant at p < 0.05. The percentage of nodular thyroid glands observed by US in each group was as follows: G1, 50%; G2, 23.8%; G3, 61%; G4, 16.1%. Again, the differences between G1 and G2 and between G3 and G4 were statistically significant ( p < 0.005 and p < 0.001, respectively, for each comparison). Conclusions: It is concluded that the higher circulating levels of insulin cause increased thyroid proliferation. The clinical manifestations are the larger thyroid volume and the formation of nodules. Thus, the thyroid gland appears to be another victim of the insulin resistance syndrome.
引用
收藏
页码:461 / 464
页数:4
相关论文
共 21 条
[1]
Diagnosing insulin resistance by simple quantitative methods in subiects with normal glucose metabolism [J].
Ascaso, JF ;
Pardo, S ;
Real, JT ;
Lorente, RI ;
Priego, A ;
Carmena, R .
DIABETES CARE, 2003, 26 (12) :3320-3325
[2]
Insulin resistance concepts [J].
Bloomgarden, Zachary T. .
DIABETES CARE, 2007, 30 (05) :1320-1326
[3]
Angiogenesis inhibitor, TNP-470, prevents diet-induced and genetic obesity in mice [J].
Bråkenhielm, E ;
Cao, RH ;
Gao, BH ;
Angelin, B ;
Cannon, B ;
Parini, P ;
Cao, YH .
CIRCULATION RESEARCH, 2004, 94 (12) :1579-1588
[4]
VOLUMETRIC-ANALYSIS OF THYROID LOBES BY REAL-TIME ULTRASOUND [J].
BRUNN, J ;
BLOCK, U ;
RUF, G ;
BOS, I ;
KUNZE, WP ;
SCRIBA, PC .
DEUTSCHE MEDIZINISCHE WOCHENSCHRIFT, 1981, 106 (41) :1338-1340
[5]
Reduction of macrophage infiltration and chemoattractant gene expression changes in white adipose tissue of morbidly obese subjects after surgery induced weight loss [J].
Cancello, R ;
Henegar, C ;
Viguerie, N ;
Taleb, S ;
Poitou, C ;
Rouault, C ;
Coupaye, M ;
Pelloux, V ;
Hugol, D ;
Bouillot, JL ;
Bouloumié, A ;
Barbatelli, G ;
Cinti, S ;
Svensson, PA ;
Barsh, GS ;
Zucker, JD ;
Basdevant, A ;
Langin, D ;
Clément, K .
DIABETES, 2005, 54 (08) :2277-2286
[6]
Adipocyte death defines macrophage localization and function in adipose tissue of obese mice and humans [J].
Cinti, S ;
Mitchell, G ;
Barbatelli, G ;
Murano, I ;
Ceresi, E ;
Faloia, E ;
Wang, SP ;
Fortier, M ;
Greenberg, AS ;
Obin, MS .
JOURNAL OF LIPID RESEARCH, 2005, 46 (11) :2347-2355
[7]
The metabolic syndrome [J].
Eckel, RH ;
Grundy, SM ;
Zimmet, PZ .
LANCET, 2005, 365 (9468) :1415-1428
[8]
Milk as a supplement to mixed meals may elevate postprandial insulinaemia [J].
Elmståhl, HL ;
Bjöorck, I .
EUROPEAN JOURNAL OF CLINICAL NUTRITION, 2001, 55 (11) :994-999
[9]
Paracrine regulation of angiogenesis and adipocyte differentiation during in vivo adipogenesis [J].
Fukumura, D ;
Ushiyama, A ;
Duda, DG ;
Xu, L ;
Tam, J ;
Chatterjee, VKK ;
Garkavtsev, I ;
Jain, RK .
CIRCULATION RESEARCH, 2003, 93 (09) :E88-E97
[10]
GROZOVSKY R, 2003, ARQ BRAS ENDOCRIN S1, V45, pS99