• Proceedings of the PSK Conference
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• 2000.04a
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• pp.152.1-152.1
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• 2000

• Proceedings of the PSK Conference
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• 2001.10a
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• pp.217.1-217.1
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• 2001

• Molecules and Cells
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• v.26 no.5
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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.

• Molecules and Cells
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• v.45 no.3
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• pp.112-121
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• 2022

Calorie restriction (CR) and the activation of autophagy extend healthspan by delaying the onset of age-associated diseases in most living organisms. Because protein kinase CK2 (CK2) downregulation induces cellular senescence and nematode aging, we investigated CK2's role in CR and autophagy. This study indicated that CR upregulated CK2's expression, thereby causing SIRT1 and AMP-activated protein kinase (AMPK) activation. CK2α overexpression, including antisense inhibitors of miR-186, miR-216b, miR-337-3p, and miR-760, stimulated autophagy initiation and nucleation markers (increase in ATG5, ATG7, LC3BII, beclin-1, and Ulk1, and decrease in SQSTM1/p62). The SIRT1 deacetylase, AKT, mammalian target of rapamycin (mTOR), AMPK, and forkhead homeobox type O (FoxO) 3a were involved in CK2-mediated autophagy. The treatment with the AKT inhibitor triciribine, the AMPK activator AICAR, or the SIRT1 activator resveratrol rescued a reduction in the expression of lgg-1 (the Caenorhabditis elegans ortholog of LC3B), bec1 (the C. elegans ortholog of beclin-1), and unc-51 (the C. elegans ortholog of Ulk1), mediated by kin-10 (the C. elegans ortholog of CK2β) knockdown in nematodes. Thus, this study indicated that CK2 acted as a positive regulator in CR and autophagy, thereby suggesting that these four miRs' antisense inhibitors can be used as CR mimetics or autophagy inducers.

• Journal of Nutrition and Health
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• v.10 no.1
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• pp.38-43
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• 1977

This study was designed to find out the status of low sodium diet in 27 hospitals located in Seoul and rural areas. The study was conducted from the beginning of June, 1976 to October, 1976. The differences in Na, protein and calorie contents between the hospitals in Seoul an ones in rural areas, and between the medical college attached hospitals and general ones, were compared by means of t-test. Correlation coefficient were made among Na, protein and calorie. In order to find out which food group is the major source of Na in the diet, six food groups were divided and Na content in each was calculated. The results showed that average daily Na intake of 27 hospitals was 2,382mg which is regarded as mild restriction. Average daily protein and calorie intakes were 94gm and 2,438 cal respectively. About 60% of hospitals restricted sodium at mild level $(2,300mg{\sim}4,600mg)$ and 33% at moderate $(1,000mg{\sim}2,300mg)$ and only 7% of the subjects were Planning strict sodium restriction $(250mg{\sim}500mg)$ There was statistically significant differences in Na contents between Seoul and rural areas. But no significant difference was found between medical college attached hospitals and general ones. The correlation between the average daily intakes of Na and protein was found not to be significant but protein and calorie intakes were related each other. When the total sodium intakes divided into six groups, about 74% were supplied by condiments (Food group 6th).

• Nutrition Research and Practice
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• v.8 no.4
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• pp.469-475
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• 2014

BACKGROUND/OBJECTIVE: The goal of the present study was to investigate the effects of moderate caloric restriction on ${\beta}$-cell function and insulin sensitivity in middle-aged obese Korean women. SUBJECTS/METHODS: Fifty-seven obese pre-menopausal Korean women participated in a 12-week calorie restriction program. Data on total cholesterol (TC), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), triglycerides (TG), and fasting serum levels of glucose, insulin, C-peptide, blood pressure, leptin and anthropometrics were collected. A dietary intake assessment was based on three days of food recording. Additionally, ${\beta}$-cell function [homeostasis model assessment of ${\beta}$-cell (HOMA-${\beta}$), insulinogenic index (ISI), C-peptide:glucose ratio, and area under curve insulin/glucose ($AUC_{ins/glu}$)] and insulin sensitivity [homeostasis model assessment for insulin resistance (HOMA-IR), Quantitative insulin-sensitivity check index (QUICKI) and Matsuda index (MI)] were recorded. RESULTS: When calories were reduced by an average of 422 kcal/day for 12 weeks, BMI (-2.7%), body fat mass (-10.2%), and waist circumference (-5%) all decreased significantly (P < 0.05). After calorie restriction, weight, body fat percentage, hip circumference, BP, TC, HDL-C, LDL-C, plasma glucose at fasting, insulin at fasting and 120 min, $AUC_{glu}$ and the insulin area under the curve all decreased significantly (all P < 0.05), while insulin sensitivity (HOMA-IR, QUICKI and Matsuda index) measured by OGTT improved significantly (P < 0.01). CONCLUSIONS: Moderate weight loss due to caloric restriction with reduction in insulin resistance improves glucose tolerance and insulin sensitivity in middle-aged obese women and thereby may help prevent the development of type 2 diabetes mellitus.

• BMB Reports
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• v.47 no.10
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• pp.587-592
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• 2014

We investigated the effects of ${\beta}$-adrenergic activation on bone marrow adiposity and on adipogenic differentiation of bone marrow mesenchymal stem cells (BMSCs). C57BL/6 mice were subjected to a control (CON), high calorie (HIGH) or low calorie (LOW) diet for 12 weeks. In each group, mice were treated with vehicle (VEH) or propranolol. The number of adipocytes per area bone marrow was increased in LOWVEH and HIGHVEH mice compared with CONVEH mice, which was attenuated by propranolol. Isoproterenol increased lipid droplet accumulation and adipogenic marker gene expression in 3T3-L1 preadipocytes and mouse BMSCs, which were blocked by propranolol. Conditioned medium obtained from MC3T3-E1 osteoblasts suppressed adipogenic differentiation of 3T3-L1 cells, which was significantly attenuated by treatment of MC3T3-E1 cells with isoproterenol. These data suggest that ${\beta}$-adrenergic activation enhances bone marrow adipogenesis via direct stimulation of BMSCs adipogenesis and indirect inhibition of osteoblast anti-adipogenic potential.

• Bulletin of the Korean Chemical Society
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• v.30 no.9
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• pp.2117-2120
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• 2009

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.173-174
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• 2002

Oxidative modification of cellular structures and functions by redox imbalance is the basis of the current oxidative stress hypothesis of aging. The experimental support for this hypothsis has been generated from recent molecular probing on the interrelation between the age-related functional impairments and the pathogenesis. (omitted)

• BMB Reports
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• v.52 no.1
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• pp.24-34
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• 2019

Sirtuin is an essential factor that delays cellular senescence and extends the organismal lifespan through the regulation of diverse cellular processes. Suppression of cellular senescence by Sirtuin is mainly mediated through delaying the age-related telomere attrition, sustaining genome integrity and promotion of DNA damage repair. In addition, Sirtuin modulates the organismal lifespan by interacting with several lifespan regulating signaling pathways including insulin/IGF-1 signaling pathway, AMP-activated protein kinase, and forkhead box O. Although still controversial, it is suggested that the prolongevity effect of Sirtuin is dependent with the level of and with the tissue expression of Sirtuin. Since Sirtuin is also believed to mediate the prolongevity effect of calorie restriction, activators of Sirtuin have attracted the attention of researchers to develop therapeutics for age-related diseases. Resveratrol, a phytochemical rich in the skin of red grapes and wine, has been actively investigated to activate Sirtuin activity with consequent beneficial effects on aging. This article reviews the evidences and controversies regarding the roles of Sirtuin on cellular senescence and lifespan extension, and summarizes the activators of Sirtuin including Sirtuin-activating compounds and compounds that increase the cellular level of nicotinamide dinucleotide.