• 한국동물학회:뉴스레터
• /
• 제12권2호
• /
• pp.94-94
• /
• 1995

No Abstract, See Full Text

• 대한약학회:학술대회논문집
• /
• 대한약학회 2001년도 Proceedings of the Pharmaceutical Society of Korea
• /
• pp.127.2-127.2
• /
• 2001

• BMB Reports
• /
• 제51권10호
• /
• pp.538-543
• /
• 2018

Pancreatic beta cell destruction and dysfunction induced by cytokines is a major cause of type 1 diabetes. Paraoxonase 1 (PON1), an arylesterase with antioxidant activity, has been shown to play an important role in preventing the development of diabetes in transgenic mice. However, no studies have examined the anti-diabetic effect of PON1 delivered to beta cells using protein transduction. In this study, we expressed the cell-permeable PON1 fused with PEP-1 protein transduction domain (PEP-1-PON1) to investigate whether transduced PEP-1-PON1 protects beta cells against cytokine-induced cytotoxicity. PEP-1-PON1 was effectively delivered to INS-1 cells and prevented cytokine-induced cell destruction in a dose-dependent manner. Transduced PEP-1-PON1 significantly reduced the levels of reactive oxygen species (ROS) and nitric oxide (NO), DNA fragmentation, and expression of inflammatory mediators, endoplasmic reticulum (ER) stress proteins, and apoptosis-related proteins in cytokine-treated cells. Moreover, transduced PEP-1-PON1 restored the decrease in basal and glucose-stimulated insulin secretion induced by cytokines. These data indicate that PEP-1-PON1 protects beta cells from cytokine-induced cytotoxicity by alleviating oxidative/nitrosative stress, ER stress, and inflammation. Thus, PEP-1-mediated PON1 transduction might be an effective method to reduce the extent of destruction and dysfunction of pancreatic beta cells in autoimmune diabetes.

• Asian-Australasian Journal of Animal Sciences
• /
• 제2권3호
• /
• pp.233-234
• /
• 1989

• BMB Reports
• /
• 제43권9호
• /
• pp.579-583
• /
• 2010

The adipocyte-derived hormone leptin regulates appetite and bone mass. Recent research demonstrates that reciprocally, osteoblasts have a role in controlling energy metabolism. Several genes expressed in osteoblasts are involved in this process, and one of them is the Esp gene. The remaining genes regulate Esp gene expression. OST-PTP, the protein name of Esp, regulates the carboxylation of osteocalcin secreted from osteoblasts, thus affecting insulin sensitivity and insulin secretion. This review provides evidence for a novel interpretation of the connection between bone and energy metabolism and expands our understanding of the novel physiology of bone beyond its classical functions.

• 대한핵의학회지
• /
• 제5권1호
• /
• pp.65-70
• /
• 1971

Blood glucose and immunoreactive insulin (IRI) were measured during oral glucose tolerance test in 15 thyrotoxic patients and 8 normal controls, to study the glucose metabolism in thyrotoxicosis. Following were the results; 1. In thyrotoxicosis, there is noticed late rise and late fall of plasma IRI durnig oral glucose tolerance test, like as phenomenon of mild diabetes mellitus. 2. When the thyrotoxic patients were divided into normal and abnormal responsive groups after the level of blood glucose by Wilkerson Criteria, no significant differences in plasma IRI levels were noticed between two groups. 3. This result may be interpreted as relative deficiency of insulin secretion from panceas and suggest genetically related defects.

• 식품산업과 영양
• /
• 제4권3호
• /
• pp.83-87
• /
• 1999

Non-insulin-dependent diabetes mellitus (NIDDM) is characterized by insulin resistance and impaired insulim secretion. The transgenic technology, in which a specific gene can be introduced or deleted to study its function, has been established. A number of transgenic mice, altered the expression of genes potentially involved in insulin action or pancreatic ${\beta}$-cell function, have recently been developed to address questions concerning NIDDM. Thransgenic mice model may help understanding the molecular basis of complex patho-physiologies of NIDDM. This review outlines the new insights obtained from the studies of transgenic mice that overxpress or show decreased expression of putative key genes involved in the regulation of insulin resistance and pancreatic ${\beta}$-cell function, therefore in the control of glucose homeostasis.

• Endocrinology and Metabolism
• /
• 제31권1호
• /
• pp.1-6
• /
• 2016

Immoderate energy intake, a sedentary lifestyle, and aging have contributed to the increased prevalence of obesity, sarcopenia, metabolic syndrome, type 2 diabetes, and cardiovascular disease. There is an urgent need for the development of novel pharmacological interventions that can target excessive fat accumulation and decreased muscle mass and/or strength. Adipokines, bioactive molecules derived from adipose tissue, are involved in the regulation of appetite and satiety, inflammation, energy expenditure, insulin resistance and secretion, glucose and lipid metabolism, and atherosclerosis. Recently, there is emerging evidence that skeletal muscle and the liver also function as endocrine organs that secrete myokines and hepatokines, respectively. Novel discoveries and research into these organokines (adipokines, myokines, and hepatokines) may lead to the development of promising biomarkers and therapeutics for cardiometabolic disease. In this review, I summarize recent data on these organokines and focus on the role of adipokines, myokines, and hepatokines in the regulation of insulin resistance, inflammation, and atherosclerosis.

• Asian-Australasian Journal of Animal Sciences
• /
• 제30권8호
• /
• pp.1190-1197
• /
• 2017

Objective: Adipose tissue is no longer considered as an inert storage organ for lipid, but instead is thought to play an active role in regulating insulin effects via secretion adipokines. However, conflicting reports have emerged regarding the effects of adipokines. In this study, we investigated the role of adipokines in glucose metabolism and insulin sensitivity in obese Bama mini-pigs. Methods: An obesity model was established in Bama mini-pigs, by feeding with high-fat and high-sucrose diet for 30 weeks. Plasma glucose and blood biochemistry levels were measured, and intravenous glucose tolerance test was performed. Adipokines, including adiponectin, interleukin-6 (IL-6), resistin and tumor necrosis factor alpha ($TNF-{\alpha}$), and glucose-induced insulin secretion were also examined by radioimmunoassay. AMP-activated protein kinase (AMPK) phosphorylation in skeletal muscle, which is a useful insulin resistance marker, was examined by immunoblotting. Additionally, associations of AMPK phosphorylation with plasma adipokines and homeostasis model assessment of insulin resistance (HOMA-IR) index were assessed by Pearce's correlation analysis. Results: Obese pigs showed hyperglycemia, high triglycerides, and insulin resistance. Adiponectin levels were significantly decreased (p<0.05) and IL-6 amounts dramatically increased (p<0.05) in obese pigs both in serum and adipose tissue, corroborating data from obese mice and humans. However, circulating resistin and $TNF-{\alpha}$ showed no difference, while the values of $TNF-{\alpha}$ in adipose tissue were significantly higher in obese pigs, also in agreement with data from obese humans but not rodent models. Moreover, strong associations of skeletal muscle AMPK phosphorylation with plasma adiponectin and HOMA-IR index were obtained. Conclusion: AMPK impairment induced by adiponectin decrease mediates insulin resistance in high-fat and high-sucrose diet induction. In addition, Bama mini-pig has the possibility of a conformable model for human metabolic diseases.

• Journal of Yeungnam Medical Science
• /
• 제18권1호
• /
• pp.94-100
• /
• 2001

연령에 따른 내당능의 감소 발생여부를 Sprague-Dawley종 흰쥐 수컷을 실험동물로 하여 연구한 결과는 다음과 같다. 연령에 따른 몸무게 변화는 1개월에서 2개월 사이에는 급격한 증가를 보였으며 2개월에서 4개월까지는 완만한 증가를 그 후 8개월까지는 미미하였다. 절식상태에서 혈당량(mg/dl)은 성장기군에서 $92{\pm}8.9$였으며 성숙기군에서는 $106{\pm}13.6$으로 성장기군에 비해 높았으며 인슐린 농도 또한 성숙기군에서 높았다. 체중 100mg당 180mg의 당을 부하한 내당능 검사에서도 성숙기군에서는 성장기군에 비해 당내성의 감소현상을 나타내었다. 당부하 검사시 동시에 측정한 혈장 인슐린 농도는 첫 30분에는 성장기군에서 높았으나, 120분에는 성숙기군에서 높은 값을 나타내었다. Soleus근의 당 섭취능은 성숙기군에서 성장기군보다 낮았으나 통계적으로 유의한 차이는 없었다. 인슐린 첨가에 의한 당 섭취능의 변화양상은 성숙기군과 성장기군 사이에 특별한 차이를 발견할 수 없었다.