• The Korean Journal of Physiology and Pharmacology
• /
• 제19권4호
• /
• pp.309-318
• /
• 2015

Alcohol consumption increases the risk of type 2 diabetes. However, its effects on prediabetes or early diabetes have not been studied. We investigated endoplasmic reticulum (ER) stress in the pancreas and liver resulting from chronic alcohol consumption in the prediabetes and early stages of diabetes. We separated Otsuka Long-Evans Tokushima Fatty (OLETF) rats, a type-2 diabetic animal model, into two groups based on diabetic stage: prediabetes and early diabetes were defined as occurrence between the ages of 11 to 16 weeks and 17 to 22 weeks, respectively. The experimental group received an ethanol-containing liquid diet for 6 weeks. An intraperitoneal glucose tolerance test was conducted after 16 and 22 weeks for the prediabetic and early diabetes groups, respectively. There were no significant differences in body weight between the control and ethanol groups. Fasting and 120-min glucose levels were lower and higher, respectively, in the ethanol group than in the control group. In prediabetes rats, alcohol induced significant expression of ER stress markers in the pancreas; however, alcohol did not affect the liver. In early diabetes rats, alcohol significantly increased most ER stress-marker levels in both the pancreas and liver. These results indicate that chronic alcohol consumption increased the risk of diabetes in prediabetic and early diabetic OLETF rats; the pancreas was more susceptible to damage than was the liver in the early diabetic stages, and the adaptive and proapoptotic pathway of ER stress may play key roles in the development and progression of diabetes affected by chronic alcohol ingestion.

• Asian-Australasian Journal of Animal Sciences
• /
• 제13권11호
• /
• pp.1529-1535
• /
• 2000

The aim of the present study was to determine whether brain corticotropin-releasing factor (CRF) and a new peptide, urocortin (UCN) have a direct action in brain mechanisms controlling feed, water and salt intake in sheep. We gave a continuous intracerebroventricular (ICV) infusion of the peptide at a small dose of $5{\mu}g/0.2ml/hr$ for 98.5 hrs from day 1 to day 5 in sheep not exposed to stress. Feed and water intake during ICV infusion of CRF or UCN decreased significantly compared to those during artificial cerebrospinal fluid (CSF) infusion. NaCl intake during infusion of CRF or UCN was the same as that during CSF infusion. Mean carotid arterial blood pressure (MAP) and heart rate during ICV infusion of CRF or UCN were not significantly different from that during CSF infusion. On the other hand, the plasma glucose concentration during ICV infusion of CRF or UCN tended to be higher than that during CSF infusion. These observations indicate that decreased feed intake induced by CRF and UCN infusion is not mediated by the activation of both the pituitary-adrenal axis and the sympathetic nervous system. The results suggested that brain CRF and UCN act directly in brain mechanisms controlling ingestive behavior to decrease feed and water intake, but do not alter salt intake in sheep.

• Molecules and Cells
• /
• 제46권8호
• /
• pp.496-512
• /
• 2023

A fructose-enriched diet is thought to contribute to hepatic injury in developing non-alcoholic steatohepatitis (NASH). However, the cellular mechanism of fructose-induced hepatic damage remains poorly understood. This study aimed to determine whether fructose induces cell death in primary hepatocytes, and if so, to establish the underlying cellular mechanisms. Our results revealed that treatment with high fructose concentrations for 48 h induced mitochondria-mediated apoptotic death in mouse primary hepatocytes (MPHs). Endoplasmic reticulum stress responses were involved in fructose-induced death as the levels of phosho-eIF2α, phospho-C-Jun-N-terminal kinase (JNK), and C/EBP homologous protein (CHOP) increased, and a chemical chaperone tauroursodeoxycholic acid (TUDCA) prevented cell death. The impaired oxidation metabolism of fatty acids was also possibly involved in the fructose-induced toxicity as treatment with an AMP-activated kinase (AMPK) activator and a PPAR-α agonist significantly protected against fructose-induced death, while carnitine palmitoyl transferase I inhibitor exacerbated the toxicity. However, uric acid-mediated toxicity was not involved in fructose-induced death as uric acid was not toxic to MPHs, and the inhibition of xanthine oxidase (a key enzyme in uric acid synthesis) did not affect cell death. On the other hand, treatment with inhibitors of the nicotinamide adenine dinucleotide (NAD)⁺-consuming enzyme CD38 or CD38 gene knockdown significantly protected against fructose-induced toxicity in MPHs, and fructose treatment increased CD38 levels. These data suggest that CD38 upregulation plays a role in hepatic injury in the fructose-enriched diet-mediated NASH. Thus, CD38 inhibition may be a promising therapeutic strategy to prevent fructose-enriched diet-mediated NASH.

• 대한의생명과학회지
• /
• 제12권4호
• /
• pp.435-438
• /
• 2006

In eukaryotes, ER stress induces UPR (unfolded protein response) via IRE1 activation which sends a molecular signal for XBP1 mRNA splicing in the cytosol. During this mRNA splicing, 23 nt removed in which contains PstI site and then resulting XBP1 product is not digested with PstI restriction enzyme. In this study, using this XBP1 mRNA splicing mechanism, the effect of heat shock on thyrocytes is studied, because heat shock response in the thyrocytes needs more study to understand thyroid physiology under alternative environments. ER inducible drugs (tunicamycin, DTT, $Ca^{2+}$ ionopore A23187, BFA) induce ER stress in the thyrocytes. From 3 hours after heat shock, ER stress is induced and which is reversible when heat shock is without. While $Ca^{2+}$ ionopore A23187 is reversible from ER stress by washing out the drug, thapsigagin is irreversible. Other ER inducible drugs are not so sensitive to ER stress repairing. XBP1 mRNA splicing in a cell is very available method to detect ER stress. It needs only a small quantity of total RNA and processing also very easy.

• Ocean and Polar Research
• /
• 제39권2호
• /
• pp.107-114
• /
• 2017

In this study, we investigated the effects of light spectra on physiology stress and DNA damage in juvenile rock bream (Oplegnathus fasciatus) using light-emitting diodes (LEDs; green, 520 nm; red, 630 nm) at two intensities (0.25 and $0.5W/m^2$ ) with application of thermal stress (25 and $30^{\circ}C$). We measured the mRNA expression of heat shock protein 70 (HSP70) and the levels of plasma cortisol, glucose, aspartate aminotransferase (AspAT), and alanine aminotransferase (AlaAT). Additionally, DNA damage was measured using comet assays. Our findings showed that HSP70 mRNA expression and plasma cortisol, glucose, AspAT, and AlaAT levels were significantly higher after exposure to high temperatures and were significantly lower after exposure to green LED light. Thus, although high water temperatures induced stress in juvenile rock bream, green LED light inhibited stress. In particular, green LED light reduced stress and DNA damage to a greater degree than other light sources.

• Animal Bioscience
• /
• 제37권6호
• /
• pp.1121-1129
• /
• 2024

Objective: Objective of the study was to reduce heat stress in Murrah buffaloes and maintain their milk production and other vital functions during heat stress. Methods: A total of 21 dyads of calf-mother Murrah buffalo were selected for the study and equally divided in 3 treatment groups. First treatment group was restricted calf contact (RCC), second treatment group was fence line calf contact (FCC) and third treatment groups fence line calf contact and heat stress protection (FCC-HSP [time-controlled fan-fogger system] in the shed). Present study was conducted from April to mid-September 2021. Results: Maximum temperature and temperature humidity index in FCC-HSP shed were significantly (p<0.05) lower than that in FCC and RCC shed. Higher (p<0.05) mean daily milk yield in both the treatment groups FCC (10.36±0.30) and FCC-HSP (10.97±0.31) than RCC (8.29±0.41) was recorded. Though no significant difference between FCC and FCC-HSP in daily milk yield but FCC-HSP yielded 600 gm more milk than FCC. Pulse rate (PR) and respiration rate (RR) were lowest in FCC-HSP followed by FCC and RCC, respectively. Cortisol and prolactin levels were lower (p<0.05) in FCC-HSP followed by FCC and RCC, respectively. Conclusion: Hence, FCC along with heat stress ameliorative measures helped the buffaloes to be free of stress and maintain milk yield during heat stress period of the year in tropical conditions.

• Tuberculosis and Respiratory Diseases
• /
• 제65권6호
• /
• pp.464-470
• /
• 2008

연구배경: 산소독에 의한 급성 폐손상에 대한 기전은 아직 확실히 알려져 있지 않다. 급성호흡곤란증후군에서 보이는 호중구의 산소기 생성에 따른 조직의 손상이 산소독에 의한 손상에서도 관여하는지를 확인하고자 하였다. 방 법: Plastic cage 내의 기압을 1기압으로 고정하고 흰쥐에게 순수한 산소를 48시간 호흡시킨 후 호중구가 폐장 내로 침윤함으로써 나타나는 급성 폐손상을 생화학적인 지표 및 형태학적인 관찰 등을 통하여 검사하였다. 결 과: 흰쥐에게 순수한 산소를 48시간 호흡하게 한 경우 폐부종, 호중구의 침윤, 폐장 내 MDA 및 $cPLA_2$ 활동도의 증가가 관찰되었고, 형태학적으로도 탐식구 특히 호중구의 침윤에 따른 폐장의 손상이 관찰되었다. 결 론: 산소독에 의한 급성폐손상의 기전은 고농도의 산소에 의한 산소기 생성이 그 원인으로 생각 되지만 산소기의 작용기전은 부분적으로 $cPLA_2$활성도 증가에 의한 호중구의 조직 내 침윤에 따른 이차적 산소기 형성이 그 원인으로 생각되며 시간이 경과할수록 호중구에 폐장 내 침윤에 따른 손상이 더 심해질 것으로 생각된다.

• 한국작물학회지
• /
• 제24권1호
• /
• pp.57-65
• /
• 1979

대.소맥에 대한 유리 Proline 축적의 온도범위, 장기저온처리의 경향, 저온과 수분부족에 있어서 광의재생의 여부 및 수종의 식물에 대한 종간 및 종내의 변이 등 일련의 반응생리와 축적기작에 대한 실험결과를 요약하면 다음과 같다. 1. 대맥은 8$^{\circ}C$나 그 이하의 온도에서 축적되나 소맥은 12$^{\circ}C$나 그 이하의 온도에서 Proline을 축적하였다. 2. 대.소맥에 있어서 신장억제온도와 Proline을 축적하기 시작하는 온도는 거의 일치하였다. 3. 엽절편을 5$^{\circ}C$의 저온에 둔 것은 29일 생존하였으며 그동안 Proline을 축적하였으나 2$0^{\circ}C$에 둔 것은 13일 밖에 생존하지 못하였으며 그 동안 축적은 없었다. 4. 완전식물체엽과 엽절편 공히 5$^{\circ}C$의 저온에 서의 축적은 광의재생이였다. 5. 광의재생은 Proline의 생합성을 위한 전구물질의 급여로는 대체될 수 없었다. 6. 수분부족에 의한 Proline 축적은 2$0^{\circ}C$에서는 광의재생이 아니였으나 5$^{\circ}C$에서는 광의재생이였다. 7. 저온과 수분부족에 대한 종간 및 종내의 축적변이는 높은 편이였다. 그러나 수분부족이 저온에 대한 변이보다 높았다. 8. 저온과 수분부족에 의한 Proline 축적의 기작은 상당히 상이한 것 같다.

• 대한약침학회지
• /
• 제22권2호
• /
• pp.83-89
• /
• 2019

Introduction: Oxidative stress (OS) during uncontrolled hyperglycemia has a pivotal role in pancreatic dysfunction. Our study aimed to demonstrate that crocin can potentiate anti-oxidant defense systems of pancreatic cells to improve oxidative stress. Methods: Male Wistar rats were divided randomly into four groups: a normal group, a normal-treated group, a diabetic group and a diabetic-treated group (n = 6 rats per group). Diabetes was induced by a single dose of streptozotocin (45 mg/kg/IV). The treated groups received crocin daily for 8 weeks (40 mg/kg/IP). At the end of the experiment, rats were sacrificed and pancreas tissue was obtained. Subsequently, the concentrations of malondialdehyde (MDA), nitrate and glutathione as well as the enzymatic activities of catalase and superoxide dismutase (SOD) were determined in all animals. Data were analyzed by two-way ANOVA with appropriate post hoc testing and a probability value of P < 0.05 was considered to represent a statistically significant difference in mean values. Results: Uncontrolled hyperglycemia weakened the anti-oxidant system by decreasing SOD and catalase enzyme activity in pancreatic tissues and induced OS by increasing the MDA content in diabetic non-treated animals. Crocin potentiated the anti-oxidant defense system by increasing the activity of both SOD and catalase, and improved OS by diminishing MDA production in pancreatic cells of rats contained in the diabetic-treated group. Conclusion: Based on our results, it is concluded that uncontrolled hyperglycemia can weaken the anti-oxidant defense system and cause the development of OS. Also, crocin can improve OS in pancreatic cells by potentiating the anti-oxidant defense system.

• 한국작물학회:학술대회논문집
• /
• 한국작물학회 2023년도 춘계학술대회
• /
• pp.112-112
• /
• 2023