Publications by authors named "Dong Joo Yang"

21 Publications

  • Page 1 of 1

Hypothalamic primary cilium: A hub for metabolic homeostasis.

Exp Mol Med 2021 Jul 1;53(7):1109-1115. Epub 2021 Jul 1.

Departments of Oral Biology and Applied Biological Science, BK21 Four, Yonsei University College of Dentistry, Seoul, 03722, Korea.

Obesity is a global health problem that is associated with adverse consequences such as the development of metabolic disorders, including cardiovascular disease, neurodegenerative disorders, and type 2 diabetes. A major cause of obesity is metabolic imbalance, which results from insufficient physical activity and excess energy intake. Understanding the pathogenesis of obesity, as well as other metabolic disorders, is important in the development of methods for prevention and therapy. The coordination of energy balance takes place in the hypothalamus, a major brain region that maintains body homeostasis. The primary cilium is an organelle that has recently received attention because of its role in controlling energy balance in the hypothalamus. Defects in proteins required for ciliary function and formation, both in humans and in mice, have been shown to cause various metabolic disorders. In this review, we provide an overview of the critical functions of primary cilia, particularly in hypothalamic areas, and briefly summarize the studies on the primary roles of cilia in specific neurons relating to metabolic homeostasis.
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http://dx.doi.org/10.1038/s12276-021-00644-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8333261PMC
July 2021

-Coumaric Acid Enhances Hypothalamic Leptin Signaling and Glucose Homeostasis in Mice via Differential Effects on AMPK Activation.

Int J Mol Sci 2021 Jan 31;22(3). Epub 2021 Jan 31.

School of Medicine, Tan Tao University, Duc Hoa 850000, Long An, Vietnam.

AMP-activated protein kinase (AMPK) plays a crucial role in the regulation of energy homeostasis in both peripheral metabolic organs and the central nervous system. Recent studies indicated that -Coumaric acid (CA), a hydroxycinnamic phenolic acid, potentially activated the peripheral AMPK pathway to exert beneficial effects on glucose metabolism in vitro. However, CA's actions on central AMPK activity and whole-body glucose homeostasis have not yet been investigated. Here, we reported that CA exhibited different effects on peripheral and central AMPK activation both in vitro and in vivo. Specifically, while CA treatment promoted hepatic AMPK activation, it showed an inhibitory effect on hypothalamic AMPK activity possibly by activating the S6 kinase. Furthermore, CA treatment enhanced hypothalamic leptin sensitivity, resulting in increased proopiomelanocortin (POMC) expression, decreased agouti-related peptide (AgRP) expression, and reduced daily food intake. Overall, CA treatment improved blood glucose control, glucose tolerance, and insulin sensitivity. Together, these results suggested that CA treatment enhanced hypothalamic leptin signaling and whole-body glucose homeostasis, possibly via its differential effects on AMPK activation.
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http://dx.doi.org/10.3390/ijms22031431DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7867021PMC
January 2021

β-Neoendorphin Enhances Wound Healing by Promoting Cell Migration in Keratinocyte.

Molecules 2020 Oct 12;25(20). Epub 2020 Oct 12.

Department of Oral Biology, Yonsei University College of Dentistry, Seoul 03722, Korea.

The skin is the largest and a remarkably plastic organ that serves as a protective barrier against environmental stimuli and injuries throughout life. Skin injuries are serious health problems, and wound healing is a critical process to replace devitalized cellular and tissue structures. Although some endogenous opioids are known to be involved in the modulation of wound healing, it remains to be determined whether the β-neoendorphin (β-NEP), an endogenous opioid, has beneficial effects on wound repair in human keratinocyte. In this study, we found that β-NEP accelerated wound repair through activation of mitogen-activated protein kinase (MAPK)/Erk1/2 signaling pathways in human keratinocytes. Moreover, the wound healing effect of β-NEP is mainly through the acceleration of keratinocyte migration without affecting cell proliferation. Therefore, our studies reveal that β-NEP plays an important role in the regulation of wound repair and suggest a therapeutic strategy to promote wound healing using β-NEP.
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http://dx.doi.org/10.3390/molecules25204640DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7587199PMC
October 2020

Ventromedial hypothalamic primary cilia control energy and skeletal homeostasis.

J Clin Invest 2021 01;131(1)

Department of Oral Biology, Yonsei University College of Dentistry, Seoul, Korea.

Dysfunction of primary cilia is related to dyshomeostasis, leading to a wide range of disorders. The ventromedial hypothalamus (VMH) is known to regulate several homeostatic processes, but those modulated specifically by VMH primary cilia are not yet known. In this study, we identify VMH primary cilia as an important organelle that maintains energy and skeletal homeostasis by modulating the autonomic nervous system. We established loss-of-function models of primary cilia in the VMH by either targeting IFT88 (IFT88-KOSF-1) using steroidogenic factor 1-Cre (SF-1-Cre) or injecting an adeno-associated virus Cre (AAV-Cre) directly into the VMH. Functional impairments of VMH primary cilia were linked to decreased sympathetic activation and central leptin resistance, which led to marked obesity and bone-density accrual. Obesity was caused by hyperphagia, decreased energy expenditure, and blunted brown fat function and was also associated with insulin and leptin resistance. The effect of bone-density accrual was independent of obesity, as it was caused by decreased sympathetic tone resulting in increased osteoblastic and decreased osteoclastic activities in the IFT88-KOSF-1 and VMH primary cilia knockdown mice. Overall, our current study identifies VMH primary cilia as a critical hypothalamic organelle that maintains energy and skeletal homeostasis.
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http://dx.doi.org/10.1172/JCI138107DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7773357PMC
January 2021

Carvedilol improves glucose tolerance and insulin sensitivity in treatment of adrenergic overdrive in high fat diet-induced obesity in mice.

PLoS One 2019 4;14(11):e0224674. Epub 2019 Nov 4.

School of Medicine, Tan Tao University, Long An, Viet Nam.

Catecholamine excess reflecting an adrenergic overdrive of the sympathetic nervous system (SNS) has been proposed to link to hyperleptinemia in obesity and may contribute to the development of metabolic disorders. However, relationship between the catecholamine level and plasma leptin in obesity has not yet been investigated. Moreover, whether pharmacological blockade of the adrenergic overdrive in obesity by the third-generation beta-blocker agents such as carvedilol could help to prevent metabolic disorders is controversial and remains to be determined. Using the high fat diet (HFD)-induced obese mouse model, we found that basal plasma norepinephrine, the principal catecholamine as an index of SNS activity, was persistently elevated and highly correlated with plasma leptin concentration during obesity development. Targeting the adrenergic overdrive from this chronic norepinephrine excess in HFD-induced obesity with carvedilol, a third-generation beta-blocker with vasodilating action, blunted the HFD-induced hepatic glucose over-production by suppressing the induction of gluconeogenic enzymes, and enhanced the muscular insulin signaling pathway. Furthermore, carvedilol treatment in HFD-induced obese mice decreased the enlargement of white adipose tissue and improved the glucose tolerance and insulin sensitivity without affecting body weight and blood glucose levels. Our results suggested that catecholamine excess in obesity might directly link to the hyperleptinemic condition and the therapeutic targeting of chronic adrenergic overdrive in obesity with carvedilol might be helpful to attenuate obesity-related metabolic disorders.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0224674PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6827914PMC
April 2020

P110β in the ventromedial hypothalamus regulates glucose and energy metabolism.

Exp Mol Med 2019 04 26;51(4):1-9. Epub 2019 Apr 26.

Division of Hypothalamic Research, Department of Internal Medicine, UT Southwestern Medical Center, Dallas, TX, 75390, USA.

Phosphoinositide 3-kinase (PI3K) signaling in hypothalamic neurons integrates peripheral metabolic cues, including leptin and insulin, to coordinate systemic glucose and energy homeostasis. PI3K is composed of different subunits, each of which has several unique isoforms. However, the role of the PI3K subunits and isoforms in the ventromedial hypothalamus (VMH), a prominent site for the regulation of glucose and energy homeostasis, is unclear. Here we investigated the role of subunit p110β in steroidogenic factor-1 (SF-1) neurons of the VMH in the regulation of metabolism. Our data demonstrate that the deletion of p110β in SF-1 neurons disrupts glucose metabolism, rendering the mice insulin resistant. In addition, the deletion of p110β in SF-1 neurons leads to the whitening of brown adipose tissues and increased susceptibility to diet-induced obesity due to blunted energy expenditure. These results highlight a critical role for p110β in the regulation of glucose and energy homeostasis via VMH neurons.
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http://dx.doi.org/10.1038/s12276-019-0249-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6486607PMC
April 2019

FoxO1 regulates leptin-induced mood behavior by targeting tyrosine hydroxylase.

Metabolism 2019 02 27;91:43-52. Epub 2018 Nov 27.

Department of Oral Biology, BK21 PLUS, Yonsei University College of Dentistry, Seoul 03722, South Korea; Department of Global Medical Science, Wonju College of Medicine, Yonsei University, Wonju 26426, South Korea; Department of Wellness & Healthy Aging, Wonju College of Medicine, Yonsei University, Wonju 26426, South Korea. Electronic address:

Purpose: While leptin has been associated with various psycho-physiological functions, the molecular network in leptin-mediated mood regulation remains elusive.

Methods: Anxiolytic behaviors and tyrosine hydroxylase (TH) levels were examined after leptin administration. Functional roles of STAT3 and FoxO1 in regulation of TH expression were investigated using in vivo and in vitro systems. A series of animal behavioral tests using dopaminergic neuron-specific FoxO1 KO (FoxO1 KO) were performed and investigated the roles of FoxO1 in regulation of mood behaviors.

Results: Here, we show that administration of leptin induces anxiolytic-like phenotype through the activation of signal transducer and activator of transcription 3 (STAT3) and the inhibition of forkhead box protein O1 (FoxO1) in dopaminergic (DA) neurons of the midbrain. Specifically, STAT3 and FoxO1 directly bind to and exert opposing effects on tyrosine hydroxylase (TH) expression, where STAT3 acts as an enhancer and FoxO1 acts as a prominent repressor. Accordingly, suppression of the prominent suppressor FoxO1 by leptin strongly increased TH expression. Furthermore, our previous results showed that specific deletion of FoxO1 in DA neurons (FoxO1 KO) led to a profound elevation of TH activity and dopamine contents. Finally, FoxO1 KO mice exhibited enhanced leptin sensitivity as well as displayed reduced anxiety- and depression-like behaviors.

Conclusions: This work establishes a novel molecular mechanism of mood behavior regulation by leptin and suggests FoxO1 suppression by leptin might be a key for leptin-induced behavioral manifestation in DA neurons.
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http://dx.doi.org/10.1016/j.metabol.2018.11.013DOI Listing
February 2019

A Novel Peptide, Nicotinyl⁻Isoleucine⁻Valine⁻Histidine (NA⁻IVH), Promotes Antioxidant Gene Expression and Wound Healing in HaCaT Cells.

Mar Drugs 2018 Aug 1;16(8). Epub 2018 Aug 1.

Department of Oral Biology, BK21 PLUS, Yonsei University College of Dentistry, Seoul 03722, Korea.

Nicotinamide (NA), a water-soluble vitamin B₃, has been shown to exert cellular-protective effects against reactive oxygen species (ROS). In order to improve the cellular-protective effects of NA, we synthesized a novel compound, nicotinyl⁻isoleucine⁻valine⁻histidine (NA⁻IVH), by combining NA with jellyfish peptides' IVH. In the present study, we examined the cellular-protective effects of the novel synthetic nicotinyl-peptide, NA⁻IVH. We found that NA⁻IVH enhances the radical scavenging activity with a robust increase of the nuclear factor (erythroid-derived 2)-like factor (Nrf2) expression in human HaCaT keratinocytes. In addition, NA⁻IVH protected the cells from hydrogen peroxide (H₂O₂)-induced cell death. Interestingly, NA⁻IVH exhibited an improved wound-healing effect in a high glucose condition, possibly through the regulation of reactive oxygen species (ROS). Collectively, our results imply that a novel nicotinyl-peptide, NA⁻IVH, has a wound-healing effect in a hyperglycemic condition, possibly by modulating excessive ROS.
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http://dx.doi.org/10.3390/md16080262DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6117656PMC
August 2018

Insulin Regulates Adrenal Steroidogenesis by Stabilizing SF-1 Activity.

Sci Rep 2018 03 22;8(1):5025. Epub 2018 Mar 22.

Departments of Pharmacology and Global Medical Science, Wonju College of Medicine, Yonsei University, Wonju, 26426, Korea.

Development of metabolic syndrome is associated with hyperactivity of the HPA axis characterized by elevated levels of circulating adrenal hormones including cortisol and aldosterone. However, the molecular mechanism leading to the dysregulation of the HPA axis is not well elucidated. In this study, we found that insulin regulates adrenal steroidogenesis by increasing the expression and activity of steroidogenic factor 1 (SF-1) both in vitro and in vivo and this insulin effect was partly through inhibition of FoxO1. Specifically, insulin increased the protein and RNA levels of SF-1 and steroidogenic target genes. Further, adrenal SF-1 expression was significantly increased by hyperactivation of insulin signaling in mice. Together with the elevated SF-1 expression in adrenal glands, hyperactivation of insulin signaling led to increased aldosterone and corticosterone levels. On the other hand, suppressing the insulin signaling using streptozotocin markedly reduced the expression of adrenal SF-1 in mice. In addition, overexpression of FoxO1 significantly suppressed SF-1 and its steroidogenic target genes implying that the positive effect of insulin on SF-1 activity might be through suppression of FoxO1 in the adrenal gland. Taken together, these results indicate that insulin regulates adrenal steroidogenesis through coordinated control of SF-1 and FoxO1.
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http://dx.doi.org/10.1038/s41598-018-23298-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5864882PMC
March 2018

4-hydroxy-3-methoxycinnamic acid regulates orexigenic peptides and hepatic glucose homeostasis through phosphorylation of FoxO1.

Exp Mol Med 2018 02 2;50(2):e437. Epub 2018 Feb 2.

Departments of Pharmacology and Global Medical Science, Wonju College of Medicine, Yonsei University, Wonju, Republic of Korea.

4-hydroxy-3-methoxycinnamic acid (ferulic acid, FA) is known to have numerous beneficial health effects, including anti-obesity and anti-hyperglycemic properties. However, the molecular networks that modulate the beneficial FA-induced metabolic effects have not been well elucidated. In this study, we explored the molecular mechanisms mediating the beneficial metabolic effects of FA. In mice, FA protected against high-fat diet-induced weight gain, reduced food intake and exhibited an overall improved metabolic phenotype. The food intake suppression by FA was accompanied by a specific reduction in hypothalamic orexigenic neuropeptides, including agouti-related protein and neuropeptide Y, with no significant changes in the anorexigenic peptides pro-opiomelanocortin and cocaine and amphetamine-regulated transcript. FA treatment also inhibited fat accumulation in the liver and white adipose tissue and suppressed the expression of gluconeogenic genes, including phosphoenolpyruvate carboxylase and glucose-6-phosphatase. Furthermore, we show that FA phosphorylated and inactivated the transcription factor FoxO1, which positively regulates the expression of gluconeogenic and orexigenic genes, providing evidence that FA might exert its beneficial metabolic effects through inhibition of FoxO1 function in the periphery and the hypothalamus.
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http://dx.doi.org/10.1038/emm.2017.253DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5903816PMC
February 2018

FoxO1 in dopaminergic neurons regulates energy homeostasis and targets tyrosine hydroxylase.

Nat Commun 2016 Sep 29;7:12733. Epub 2016 Sep 29.

Department of Pharmacology, Wonju College of Medicine, Yonsei University, Wonju 26426, Korea.

Dopaminergic (DA) neurons are involved in the integration of neuronal and hormonal signals to regulate food consumption and energy balance. Forkhead transcriptional factor O1 (FoxO1) in the hypothalamus plays a crucial role in mediation of leptin and insulin function. However, the homoeostatic role of FoxO1 in DA system has not been investigated. Here we report that FoxO1 is highly expressed in DA neurons and mice lacking FoxO1 specifically in the DA neurons (FoxO1 KO) show markedly increased energy expenditure and interscapular brown adipose tissue (iBAT) thermogenesis accompanied by reduced fat mass and improved glucose/insulin homoeostasis. Moreover, FoxO1 KO mice exhibit an increased sucrose preference in concomitance with higher dopamine and norepinephrine levels. Finally, we found that FoxO1 directly targets and negatively regulates tyrosine hydroxylase (TH) expression, the rate-limiting enzyme of the catecholamine synthesis, delineating a mechanism for the KO phenotypes. Collectively, these results suggest that FoxO1 in DA neurons is an important transcriptional factor that directs the coordinated control of energy balance, thermogenesis and glucose homoeostasis.
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http://dx.doi.org/10.1038/ncomms12733DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5056402PMC
September 2016

Steroidogenic Factor 1 in the Ventromedial Nucleus of the Hypothalamus Regulates Age-Dependent Obesity.

PLoS One 2016 6;11(9):e0162352. Epub 2016 Sep 6.

Departments of Pharmacology and Global Medical Science, Wonju College of Medicine, Yonsei University, Wonju, 26426, Republic of Korea.

The ventromedial nucleus of the hypothalamus (VMH) is important for the regulation of whole body energy homeostasis and lesions in the VMH are reported to result in massive weight gain. The nuclear receptor steroidogenic factor 1 (SF-1) is a known VMH marker as it is exclusively expressed in the VMH region of the brain. SF-1 plays a critical role not only in the development of VMH but also in its physiological functions. In this study, we generated prenatal VMH-specific SF-1 KO mice and investigated age-dependent energy homeostasis regulation by SF-1. Deletion of SF-1 in the VMH resulted in dysregulated insulin and leptin homeostasis and late onset obesity due to increased food intake under normal chow and high fat diet conditions. In addition, SF-1 ablation was accompanied by a marked reduction in energy expenditure and physical activity and this effect was significantly pronounced in the aged mice. Taken together, our data indicates that SF-1 is a key component in the VMH-mediated regulation of energy homeostasis and implies that SF-1 plays a protective role against metabolic stressors including aging and high fat diet.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0162352PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5012732PMC
August 2017

Hypothalamic AMPK as a Regulator of Energy Homeostasis.

Neural Plast 2016 28;2016:2754078. Epub 2016 Jul 28.

Departments of Pharmacology and Global Medical Science, Wonju College of Medicine, Yonsei University, Wonju 26426, Republic of Korea.

Activated in energy depletion conditions, AMP-activated protein kinase (AMPK) acts as a cellular energy sensor and regulator in both central nervous system and peripheral organs. Hypothalamic AMPK restores energy balance by promoting feeding behavior to increase energy intake, increasing glucose production, and reducing thermogenesis to decrease energy output. Besides energy state, many hormones have been shown to act in concert with AMPK to mediate their anorexigenic and orexigenic central effects as well as thermogenic influences. Here we explore the factors that affect hypothalamic AMPK activity and give the underlying mechanisms for the role of central AMPK in energy homeostasis together with the physiological effects of hypothalamic AMPK on energy balance restoration.
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http://dx.doi.org/10.1155/2016/2754078DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4980534PMC
October 2017

Gallic Acid Promotes Wound Healing in Normal and Hyperglucidic Conditions.

Molecules 2016 Jul 8;21(7). Epub 2016 Jul 8.

Department of Pharmacology, Wonju College of Medicine, Yonsei University, Wonju 26426, Korea.

Skin is the outermost layer of the human body that is constantly exposed to environmental stressors, such as UV radiation and toxic chemicals, and is susceptible to mechanical wounding and injury. The ability of the skin to repair injuries is paramount for survival and it is disrupted in a spectrum of disorders leading to skin pathologies. Diabetic patients often suffer from chronic, impaired wound healing, which facilitate bacterial infections and necessitate amputation. Here, we studied the effects of gallic acid (GA, 3,4,5-trihydroxybenzoic acid; a plant-derived polyphenolic compound) on would healing in normal and hyperglucidic conditions, to mimic diabetes, in human keratinocytes and fibroblasts. Our study reveals that GA is a potential antioxidant that directly upregulates the expression of antioxidant genes. In addition, GA accelerated cell migration of keratinocytes and fibroblasts in both normal and hyperglucidic conditions. Further, GA treatment activated factors known to be hallmarks of wound healing, such as focal adhesion kinases (FAK), c-Jun N-terminal kinases (JNK), and extracellular signal-regulated kinases (Erk), underpinning the beneficial role of GA in wound repair. Therefore, our results demonstrate that GA might be a viable wound healing agent and a potential intervention to treat wounds resulting from metabolic complications.
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http://dx.doi.org/10.3390/molecules21070899DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6274221PMC
July 2016

Leucine-enkephalin promotes wound repair through the regulation of hemidesmosome dynamics and matrix metalloprotease.

Peptides 2016 Feb 4;76:57-64. Epub 2016 Jan 4.

Department of Pharmacology, Wonju College of Medicine, Yonsei University, Wonju 26426, Republic of Korea; Department of Global Medical Science, Wonju College of Medicine, Yonsei University, Wonju 26426, Republic of Korea. Electronic address:

The skin responds to environmental stressors by coordinated actions of neuropeptides and their receptors. An endogenous peptide for δ-opioid receptor (DOPr), Leu-enkephalin (L-ENK), is expressed in the skin and its expression is altered in pathological conditions. Although the importance of DOPr is rapidly gaining recognition, the molecular mechanisms underlying its effects on wound healing are largely undefined. We show here that L-ENK induced activation of Erk, P90(RSK), and Elk-1 and promoted the disruption of hemidesmosomes and the expression of matrix metalloprotease (MMP)-2 and MMP-9, important processes for wound healing. Treatment with Erk inhibitor blocked activation of P90(RSK) and Elk-1 and significantly blunted wound repair. Therefore, our results suggest that activation of Erk and its downstream effectors, P90(RSK) and Elk-1, are critical for DOPr-mediated skin homeostasis.
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http://dx.doi.org/10.1016/j.peptides.2015.12.010DOI Listing
February 2016

Nutritional conditions regulate transcriptional activity of SF-1 by controlling sumoylation and ubiquitination.

Sci Rep 2016 Jan 11;6:19143. Epub 2016 Jan 11.

Departments of Pharmacology and Internal Medicine, Division of Hypothalamic Research, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.

Steroidogenic factor 1 (SF-1) is a transcription factor expressed in the ventral medial nucleus of the hypothalamus that regulates energy homeostasis. However, the molecular mechanisms of SF-1 in the control of energy balance are largely unknown. Here, we show that nutritional conditions, such as the presence or absence of serum, affect SF-1 action. Serum starvation significantly decreased hypothalamic SF-1 levels by promoting ubiquitin-dependent degradation, and sumoylation was required for this process. SF-1 transcriptional activity was also differentially regulated by nutritional status. Under normal conditions, the transcriptional activity of hypothalamic SF-1 was activated by SUMO, but this was attenuated during starvation. Taken together, these results indicate that sumoylation and ubiquitination play crucial roles in the regulation of SF-1 function and that these effects are dependent on nutritional conditions, further supporting the importance of SF-1 in the control of energy homeostasis.
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http://dx.doi.org/10.1038/srep19143DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4707483PMC
January 2016

Mycosporine-Like Amino Acids Promote Wound Healing through Focal Adhesion Kinase (FAK) and Mitogen-Activated Protein Kinases (MAP Kinases) Signaling Pathway in Keratinocytes.

Mar Drugs 2015 Nov 26;13(12):7055-66. Epub 2015 Nov 26.

Departments of Pharmacology and Global Medical Science, Wonju College of Medicine, Yonsei University, Wonju 220-701, Korea.

Mycosporine-like amino acids (MAAs) are secondary metabolites found in diverse marine, freshwater, and terrestrial organisms. Evidence suggests that MAAs have several beneficial effects on skin homeostasis such as protection against UV radiation and reactive oxygen species (ROS). In addition, MAAs are also involved in the modulation of skin fibroblasts proliferation. However, the regulatory function of MAAs on wound repair in human skin is not yet clearly elucidated. To investigate the roles of MAAs on the wound healing process in human keratinocytes, three MAAs, Shinorine (SH), Mycosporine-glycine (M-Gly), and Porphyra (P334) were purified from Chlamydomonas hedlyei and Porphyra yezoensis. We found that SH, M-Gly, and P334 have significant effects on the wound healing process in human keratinocytes and these effects were mediated by activation of focal adhesion kinases (FAK), extracellular signal-regulated kinases (ERK), and c-Jun N-terminal kinases (JNK). These results suggest that MAAs accelerate wound repair by activating the FAK-MAPK signaling pathways. This study also indicates that MAAs can act as a new wound healing agent and further suggests that MAAs might be a novel biomaterial for wound healing therapies.
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http://dx.doi.org/10.3390/md13127056DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4699230PMC
November 2015

Comparison of Physical Fitness Status between Middle-aged and Elderly Male Laborers According to Lifestyle Behaviors.

J Phys Ther Sci 2014 Dec 25;26(12):1965-9. Epub 2014 Dec 25.

Department of Occupational Therapy, College of Biomedical Sciences and Engineering, Inje University, Republic of Korea.

[Purpose] We sought to examine the relationship between lifestyle behavior and physical fitness in middle-aged and elderly laborers. [Subjects] In total, 2,469 male laborers between 45 and 64 years of age residing in eight cities in South Korea were studied between January and December 2007. [Methods] Age, height, and weight were evaluated as general characteristics. Lifestyle behavior items included exercise, dietary habits, smoking, drinking, and sleeping hours. Physical fitness was assessed by measuring muscle strength, muscle endurance, flexibility, reflexes, and agility. [Results] In terms of physical fitness status, all items except handgrip strength showed significant changes according to exercise frequency. Dietary habits were associated with significant differences in the Sargent jump and whole-body reaction time between groups. Smoking and drinking were associated with significant differences in sit-ups between subgroups. Sleeping hours demonstrated significant differences in the Sargent jump and whole-body reaction time between groups. [Conclusion] Although there were differences according to physical fitness status, exercise frequency, dietary habits, smoking, drinking, and sleeping hours showed significant associations with physical fitness. Thus, healthy lifestyle behaviors, such as regular exercise, regular dietary habits, not smoking, moderate drinking, and adequate sleep, are important for physical fitness management and work capacity improvement in middle-aged and elderly laborers.
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http://dx.doi.org/10.1589/jpts.26.1965DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4273069PMC
December 2014

Gallic acid regulates body weight and glucose homeostasis through AMPK activation.

Endocrinology 2015 Jan;156(1):157-68

Departments of Pharmacology and Global Medical Science (K.V.D., C.M.K., A.W.K., D.J.Y., Y.-H.C., I.Y.O., N.M.N., A.K., J.W.C., K.W.K.), Institute of Lifestyle Medicine and Nuclear Receptor Research Consortium (D.V.K., D.J.Y., Y.-H.C., K.W.K.), and Departments of Biochemistry (Y.J.), Anatomy (M.H.J., W.G.C.), and Physiology (S.X., K.S.P.), Yonsei University Wonju College of Medicine, Wonju 220-701, Republic of Korea; Global Research Laboratory (W.J.P.), Gwangju Institute of Science and Technology, Gwangju 500-757, Republic of Korea; Innoplant Co, Ltd (S.Y.C.), Jinju, Gyeongnam 660-844, Republic of Korea; and Antiaging Research Institute of BIO-FD & C Co Ltd (H.S.K., S.H.M., Y.-H.C.), Incheon 406-840, Republic of Korea.

Gallic acid [3,4,5-trihydroxybenzoic acid (GA)], a natural phytochemical, is known to have a variety of cellular functions including beneficial effects on metabolic syndromes. However, the molecular mechanism by which GA exerts its beneficial effects is not known. Here we report that GA plays its role through the activation of AMP-activated protein kinase (AMPK) and by regulating mitochondrial function via the activation of peroxisome proliferator-activated receptor-γ coactivator1α (PGC1α). Sirtuin 1 (Sirt1) knockdown significantly blunted GA's effect on PGC1α activation and downstream genes, suggesting a critical role of the AMPK/Sirt1/PGC1α pathway in GA's action. Moreover, diet-induced obese mice treated with GA showed significantly improved glucose and insulin homeostasis. In addition, the administration of GA protected diet-induced body weight gain without a change in food intake. Biochemical analyses revealed a marked activation of AMPK in the liver, muscle, and interscapular brown adipose tissue of the GA-treated mice. Moreover, uncoupling protein 1 together with other genes related to energy expenditure was significantly elevated in the interscapular brown adipose tissue. Taken together, these results indicate that GA plays its beneficial metabolic roles by activating the AMPK/Sirt1/PGC1α pathway and by changing the interscapular brown adipose tissue genes related to thermogenesis. Our study points out that targeting the activation of the AMPK/Sirt1/PGC1α pathway by GA or its derivatives might be a potential therapeutic intervention for insulin resistance in metabolic diseases.
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http://dx.doi.org/10.1210/en.2014-1354DOI Listing
January 2015

Reliability of self-administered Work Ability Index questionnaire among Korean workers.

Ergonomics 2013 24;56(11):1652-7. Epub 2013 Sep 24.

a Korea Safety Promotion Association , Seoul , Republic of Korea.

Although the Work Ability Index (WAI) has been used in many countries, its reliability is yet to be validated in Korea. In our study, test-retest results of WAI total score, WAI category and seven subscales were compared. The correlation coefficients of WAI total score and subscales 1 and 2 between test and retest were 0.70, 0.80 and 0.63, respectively. The κ values on WAI category, subscales 4, 5, 6 and 7 were 0.52, 0.32, 0.31, 0.48 and 0.85, respectively. The results of our reliability test show that WAI scores of female, younger and private company workers were found to be higher than those of male, older and public company workers, respectively. We conclude that overall test-retest reliability of WAI in Korea is acceptable. Another notable observation from our study is that work ability dimension (subscales 1, 2 and 7) had a higher reliability, whereas health dimension (subscales 3-6) had a lower reliability.
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http://dx.doi.org/10.1080/00140139.2013.835073DOI Listing
August 2014

Characterization of TiN coating layers using ultrasonic backward radiation.

Ultrasonics 2006 Dec 6;44 Suppl 1:e1083-7. Epub 2006 Jun 6.

School of Mechanical Engineering, Sungkyunkwan University, Suwon 440-746, Republic of Korea.

Since ceramic layers coated on machinery components inevitably experience the changes in their properties it is necessary to evaluate the characteristics of ceramic coating layers nondestructively for the reliable use of coated components and the remaining life prediction. To address such a need, in the present study, the ultrasonic backward radiation technique is applied to examine the very thin TiN ceramic layers coated on AISI 1045 steel or austenitic 304 steel substrate. Specifically, the ultrasonic backward radiation profiles have been measured with variations in specimen preparation conditions such as coating layer thickness and sliding loading. In the experiments performed in the current study, the peak angle and the peak amplitude of ultrasonic backward radiation profile varied sensitively according to two specimen preparation conditions. In fact, this result demonstrates a high possibility of the ultrasonic backward radiation as an effective tool for the nondestructive characterization of the TiN ceramic coating layers even in such a thin regime.
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http://dx.doi.org/10.1016/j.ultras.2006.05.104DOI Listing
December 2006
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