• Asian Pacific Journal of Cancer Prevention
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• 제13권1호
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• pp.139-146
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• 2012

Obese postmenopausal women increase their risk of developing breast cancer (BC), in particular if they display an android-type pattern of adiposity, which is also associated to increased risks of diabetes mellitus, hypertension and cardiovascular disease. In order to explore the associations among anthropometry (body mass index, body composition, somatotype), some specific items of medical history (diabetes, hypertension, dislypidemias, hyperuricemia) and the risk of BC in Uruguayan women, a case-control study was carried out between 2004-2009 at our Oncology Unit. 912 women of ages between 23-69 years (367 new BC cases and 545 non hospitalized, age-matched controls with a normal mammography) were interviewed. Twenty body measurements were taken in order to calculate body composition and somatotype. Patients were queried on socio-demographics, reproductive history, family history of cancer, a brief food frequency questionnaire and on personal history of diabetes, dislypidemias, hyperuricemia, hypertension and gallbladder stones. Uni- and multivariate analyses were done, generating odds ratios (ORs) as an expression of relative risks. A personal history of diabetes was positively associated to BC risk (OR=1.64, 95% CI 1.00-2.69), being higher among postmenopausal women (OR=1.92, 95% CI 1.04-3.52). The risks of BC for diabetes in postmenopausal women with overweight combined with dislypidemia (OR=9.33, 95% CI 2.10-41.5) and high fat/muscle ratio (OR=7.81, 95% CI 2.01-30.3) were significantly high. As a conclusion, a personal history of diabetes and overweight was strongly associated to BC. The studied sample had a subset of high-risk of BC featured by postmenopausal overweight and diabetic women, who also had a personal history of hypertension and/or dyslipidemia. The present results could contribute to define new high risk groups and individuals for primary as well as for secondary prevention, since this pattern linked to the metabolic syndrome is usually not considered for BC prevention.

• 대한수의학회지
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• 제44권3호
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• pp.349-355
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• 2004

The aim of this study was to evaluate the expression of galectin-3, one of beta-galactoside-binding proteins, in the experimental autoimmune encephalomyelitis(EAE) model of Lewis rats or non-obese diabetic (NOD) mice. Western blot analysis showed that galectin-3 was weakly expressed in the spinal cords of complete Freund's adjuvant(CFA) immunized control rats. In EAE, however, galectin-3 expression was significantly increased at the peak stage(days 14 post-immunization), while it was decreased slightly at the recovery stage(day 21 post-immunization). Immunohistochemical analysis showed that galectin-3 was detected in some macrophages in demyelinating lesions of NOD mice, while galectin-3 was immunoreacted in some inflammatory cells in the perivascular cuffing in rat EAE lesions. Collectively, it is postulated that the expression of galectin-3 is significantly increased in response to neuroimmunological stimulation in the central nervous system, whereas it is weak in normal rats and mice.

• Journal of Yeungnam Medical Science
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• 제4권2호
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• pp.65-73
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• 1987

1983년 5월부터 1984년 7월까지 영남대학교 의과대학 부속병원의 컴퓨터자동화 건강센터에 내원하였던 3,088명을 대상으로 하여 당뇨병의 유병율 및 당뇨병과 여러 인자들 특히 비만증과의 상관관계를 통계 분석하여 다음과 같은 결과를 얻었다. 1) 당뇨병과 당내성 장애군의 유병율은 각각 2.3%와 18.3%이다. 2) 성별에 다른 당뇨병의 유병율은 남자가 2.6%, 여자 1.7%로 남녀간에 통계적으로 유의한 차는 없었다. 3) 당뇨병의 유병율은 10대에서 70대까지 각각 0%, 0.45%, 0.67%, 3.47%, 5.36%, 10%로써 나이가 증가함에 따라 증가하는 경향이 있었다. 4) 정상군과 당뇨병군에서 비만증의 빈도는 각각 18.03%, 22.86%로써 통계학적으로 의의가 없었다($P{\geq}0.1$). 5) 비만증과 비만증군에서 당내성 장애 및 당뇨병의 유병율응 통계학적으로 의의가 없었다($P{\geq}0.1$). 6) 당내성이 감소함에 따라 단백뇨, 고BUN혈증 및 고혈압의 빈도는 유의한 증가가 있었다($P{\leq}0.05$).

• Archives of Pharmacal Research
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• 제22권5호
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• pp.437-447
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• 1999

Type I diabetes, also known as insulin-dependent diabetes mellitus (IDDM) results from the destruction of insulin-producing pancreatic $\beta$ cells by a progressive $\beta$ cell-specific autoimmune process. The pathogenesis of autoimmune IDDM has been extensively studied for the past two decades using animal models such as the non-obese diabetic (NOD) mouse and the Bio-Breeding (BB) rat. However, the initial events that trigger the immune responses leading to the selective destruction of the $\beta$ cells are poorly understood. It is thought that $\beta$ cell auto-antigens are involved in the triggering of $\beta$ cell-specific autoimmunity. Among a dozen putative $\beta$ cell autoantigens, glutamic acid decarboxylase (GAD) has bee proposed as perhaps the strongest candidate in both humans and the NOD mouse. In the NOD mouse, GAD, as compared with other $\beta$ cell autoantigens, provokes the earliest T cell proliferative response. The suppression of GAD expression in the $\beta$ cells results in the prevention of autoimmune diabetes in NOD mice. In addition, the major populations of cells infiltrating the iselts during the early stage of insulitis in BB rats and NOD mice are macrophages and dendritic cells. The inactivation of macrophages in NOD mice results in the prevention of T cell mediated autoimmune diabetes. Macrophages are primary contributors to the creation of the immune environment conducive to the development and activation of $\beta$cell-specific Th1-type CD4+ T cells and CD8+ cytotoxic T cells that cause autoimmune diabetes in NOD mice. CD4+ and CD8+ T cells are both believed to be important for the destruction of $\beta$ cells. These cells, as final effectors, can kill the insulin-producing $\beta$ cells by the induction of apoptosis. In addition, CD8+ cytotoxic T cells release granzyme and cytolysin (perforin), which are also toxic to $\beta$ cells. In this way, macrophages, CD4+ T cells and CD8+ T cells act synergistically to kill the $\beta$ cells in conjunction with $\beta$ cell autoantigens and MHC class I and II antigens, resulting in the onset of autoimmune type I diabetes.

• Journal of Korean Neurosurgical Society
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• 제65권6호
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• pp.790-800
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• 2022

Objective : EID3 (EP300-interacting inhibitor of differentiation) was identified as a novel member of EID family and plays a pivotal role in colorectal cancer development. However, its role in glioma remained elusive. In current study, we identified EID3 as a novel oncogenic molecule in human glioma and is critical for glioma cell survival, proliferation and invasion. Methods : A total of five patients with glioma were recruited in present study and fresh glioma samples were removed from patients. Four weeks old male non-obese diabetic severe combined immune deficiency (NOD/SCID) mice were used as transplant recipient models. The subcutaneous tumor size was calculated and recorded every week with vernier caliper. EID3 and AMP-activated protein kinase α1 (AMPKα1) expression levels were confirmed by real-time polymerase chain reaction and Western blot assays. Colony formation assays were performed to evaluate cell proliferation. Methyl thiazolyl tetrazolium (MTT) assays were performed for cell viability assessment. Trypan blue staining approach was applied for cell death assessment. Cell Apoptosis DNA ELISA Detection Kit was used for apoptosis assessment. Results : EID3 was preferentially expressed in glioma tissues/cells, while undetectable in astrocytes, neuronal cells, or normal brain tissues. EID3 knocking down significantly hindered glioma cell proliferation and invasion, as well as induced reduction of cell viability, apoptosis and cell death. EID3 knocking down also greatly inhibited tumor growth in SCID mice. Knocking down of AMPKα1 could effectively rescue glioma cells from apoptosis and cell death caused by EID3 absence, indicating that AMPKα1 acted as a key downstream regulator of EID3 and mediated suppression effects caused by EID3 knocking down inhibition. These findings were confirmed in glioma cells generated patient-derived xenograft models. AMPKα1 protein levels were affected by MG132 treatment in glioma, which suggested EID3 might down regulate AMPKα1 through protein degradation. Conclusion : Collectively, our study demonstrated that EID3 promoted glioma cell proliferation and survival by inhibiting AMPKα1 expression. Targeting EID3 might represent a promising strategy for treating glioma.

• 한국식품영양과학회지
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• 제41권3호
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• pp.339-344
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• 2012

본 연구에서는 제2형 당뇨병 모델인 C57BLKS/J-db/db 마우스에서 발아일품벼 추출물의 농도별로 급여한 후 혈당 조절에 미치는 영향을 알아보고자 조사하였다. C57BLKS/J-db/db 마우스에게 급여한 발아일품벼 추출물의 양에 따라 5군 즉, 정상군(Normal Control: NC), 당뇨대조군(Diabetic Control: DC), 1% 발아벼 추출물 급여군(DM-1% GIRRE), 0.5% 발아벼 추출물 급여군(DM-0.5%GIRRE), 0.25% 발아벼 추출물 급여군(DM-0.25%GIRRE)으로 나누었다. 8주 동안 매일 식이 섭취량과 음료섭취량 및 매주 체중과 공복혈당을 측정하고 마지막 주에 경구포도당 부하검사(OGTT)를 실시하였으며, 부검 시 혈액을 채취하여 혈청인슐린 농도와 당화혈색소를 측정하였다. 그 결과, DM-1% GIRRE군에서 당뇨유발에 의한 체중감소 및 당뇨 증상 중에 다음(poly-dipsia), 다식(polyphasia) 등이 어느 정도 완화되고 있음을 알 수 있다. DM-1%GIRRE군에서 당뇨동물의 공복 혈당, 경구 내당능 검사, 혈중 HbA1c 수준을 유의적으로 낮추었지만, 혈장 인슐린 농도는 당뇨실험군들 간에는 차이가 나타나지 않았다. 이상의 결과를 종합해보면 발아일품벼추출물의 급여가 혈당상승을 억제하는 효과가 있는 것으로 생각되며 그 기전에 대해서는 향후 추가 연구가 필요하다고 본다.