• 식품기술
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• 제23권3호
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• pp.400-406
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• 2010

TOR(target of rapamycin)은 모든 진행세포에서 성장과 대사를 조절하는 영양소 인식 단백질 인산화효소(nutrient-sensing protein kinase)로 곤충, 효모, 마우스를 이용한 실험 결과 TOR 신호 전달계는 노화를 조절하는 것으로 밝혀졌다. 또한 TOR은 식이제한 시 나타나는 다양한 보호 효과(생명 연장, 노화 관련 질환 발병 억제 등)의 강력한 중계자로 알려졌다. 본 리뷰에서는 TOR 신호 전달계가 어떻게 노화를 지연시키는가에 대해 다루고자 한다. 노화조절인자로서의 TOR 신호전달계 조절 기전 구명은 매우 중요한 연구 분야이며 노화 관련 질환을 타겟으로 한 제약 및 건강기능식품의 개발을 통해 인간 수명 연장의 꿈을 성취하는 것을 조금 더 앞당길 수 있을 것으로 사료된다.

• Journal of Microbiology and Biotechnology
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• 제33권5호
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• pp.680-686
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• 2023

Aging is a complex series of multi-organ processes that occur in various organisms. As such, an in vivo study using an animal model of aging is necessary to define its exact mechanisms and identify anti-aging substances. Using Drosophila as an in vivo model system, we identified Crataegus pinnatifida extract (CPE) as a novel anti-aging substance. Regardless of sex, Drosophila treated with CPE showed a significantly increased lifespan compared to those without CPE. In this study, we also evaluated the involvement of CPE in aging-related biochemical pathways, including TOR, stem cell generation, and antioxidative effects, and found that the representative genes of each pathway were induced by CPE administration. CPE administration did not result in significant differences in fecundity, locomotion, feeding amount, or TAG level. These conclusions suggest that CPE is a good candidate as an anti-aging food substance capable of promoting a healthy lifespan.

• Molecules and Cells
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• 제26권5호
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• pp.427-435
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• 2008

In this review, we discuss the genes and the related signal pathways that regulate aging and longevity by reviewing recent findings of genetic longevity models in rodents in reference to findings with lower organisms. We also paid special attention to the genes and signals mediating the effects of calorie restriction (CR), a powerful intervention that slows the aging process and extends the lifespan in a range of organisms. An evolutionary view emphasizes the roles of nutrient-sensing and neuroendocrine adaptation to food shortage as the mechanisms underlying the effects of CR. Genetic and non-genetic interventions without CR suggest a role for single or combined hormonal signals that partly mediate the effect of CR. Longevity genes fall into two categories, genes relevant to nutrient-sensing systems and those associated with mitochondrial function or redox regulation. In mammals, disrupted or reduced growth hormone (GH)-insulin-like growth factor (IGF)-1 signaling robustly favors longevity. CR also suppresses the GH-IGF-1 axis, indicating the importance of this signal pathway. Surprisingly, there are very few longevity models to evaluate the enhanced anti-oxidative mechanism, while there is substantial evidence supporting the oxidative stress and damage theory of aging. Either increased or reduced mitochondrial function may extend the lifespan. The role of redox regulation and mitochondrial function in CR remains to be elucidated.

• Journal of Microbiology and Biotechnology
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• 제23권11호
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• pp.1569-1576
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• 2013

In mice, supplementation of t10,c12 conjugated linoleic acid (CLA) increases liver mass and hepatic steatosis via increasing uptake of fatty acids released from adipose tissues. However, the effects of t10,c12 CLA on hepatic lipid synthesis and the associated mechanisms are largely unknown. Thus, we tested the hypothesis that gut microbiota-producing t10,c12 CLA would induce de novo lipogenesis and triglyceride (TG) synthesis in HepG2 cells, promoting lipid accumulation. It was found that treatment with t10,c12 CLA ($100{\mu}M$) for 72 h increased neutral lipid accumulation via enhanced incorporation of acetate, palmitate, oleate, and 2-deoxyglucose into TG. Furthermore, treatment with t10,c12 CLA led to increased mRNA expression and protein levels of lipogenic genes including SREBP1, ACC1, FASN, ELOVL6, GPAT1, and DGAT1, presenting potential mechanisms by which CLA may increase lipid deposition. Most strikingly, t10,c12 CLA treatment for 3 h increased phosphorylation of mTOR, S6K, and S6. Taken together, gut microbiota-producing t10,c12 CLA activates hepatic de novo lipogenesis and TG synthesis through activation of the mTOR/SREBP1 pathway, with consequent lipid accumulation in HepG2 cells.