• Clinical and Experimental Pediatrics
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• v.48 no.2
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• pp.126-137
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• 2005

New insights in the complex metabolic pathways and its control mechanism for energy homeostasis have refined our understanding of the pathophysiology of obesity. It is now recognized that there are several additional regulatory mechanism such as peripheral signals including leptin, ghrelin, GLP-1 and PYY and cellular signals including uncoupling proteins and ${\beta}$ Adrenergic receptors, which contribute to the regulation of food intake and energy expenditure, respectively. In addition, the function of adipocyte as an endocrine organ in energy homeostasis has been recently emphasized. Recent findings suggest that elevated levels of adipokines, such as leptin, adiponectin, resistin and TNF-${\alpha}$, in addition to increased free fatty acid level could be related to the pathophysiology of insulin resistance in obesity. For effective treatments and prevention of obesity, further studies on the circuits of neural and endocrine interactions in the regulation of energy homeostasis are needed.

• Molecules and Cells
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• v.38 no.12
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• pp.1023-1028
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• 2015

Whole body energy balance is achieved through the coordinated regulation of energy intake and energy expenditure in various tissues including liver, muscle and adipose tissues. A positive energy imbalance by excessive energy intake or insufficient energy expenditure results in obesity and related metabolic diseases. Although there have been many obesity treatment trials aimed at the reduction of energy intake, these strategies have achieved only limited success because of their associated adverse effects. An ancient neurotransmitter, serotonin is among those traditional pharmacological targets for anti-obesity treatment because it exhibits strong anorectic effect in the brain. However, recent studies suggest the new functions of peripheral serotonin in energy homeostasis ranging from the endocrine regulation by gut-derived serotonin to the autocrine/paracrine regulation by adipocyte-derived serotonin. Here, we discuss the role of serotonin in the regulation of energy homeostasis and introduce peripheral serotonin as a possible target for anti-obesity treatment.

• International Journal of Oral Biology
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• v.34 no.2
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• pp.49-52
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• 2009

Perception of sweet compounds is important for animals to detect external carbohydrate source of calories and plays a crucial role in feeding behavior of animals. Recent progress in molecular genetic studies provides evidence for a candidate receptor (heterodimers with taste receptor type 1 member 2 and 3: T1R2/T1R3), and major downstream transduction molecules required for sweet taste signaling. Several studies demonstrated that the sweet taste signal can be modulated by a satiety hormone, leptin, through its receptors expressed in a subset of sweet-sensitive taste cells. Increase of internal energy storage in the adipose tissue leads to increase in the plasma leptin level which can reduce activities of sweet-sensitive cells. In human, thus, diurnal variation of plasma leptin level parallels variation of taste recognition thresholds for sweet compounds. This leptin modulation of sweet taste sensitivity may influence individuals' preference, ingestive behavior, and absorption of nutrients, thereby plays important roles in regulation of energy homeostasis.

• Natural Product Sciences
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• v.25 no.2
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• pp.165-171
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• 2019

Although the functions of a standardized extract of Gingko biloba leaves (EGb $761^{(R)}$) has been reported with regard to neurobiological properties, no attention has been paid to the impact of EGb $761^{(R)}$ on the neuronal regulation of energy homeostasis. To evaluate the hypothesis that EGb $761^{(R)}$ affect the secretion of peptide tyrosine tyrosine (PYY) and the activation of free fatty acid receptor 4 (FFA4), which are involved in the neuronal circuitries that control energy homeostasis by inducing the transfer of information about the influx of energy to the brain, we examined whether EGb $761^{(R)}$ can stimulate PYY secretion in the enteroendocrine NCI-H716 cells and if EGb $761^{(R)}$ can activate FFA4 in FFA4-expressing cells. In NCI-H716 cells, EGb $761^{(R)}$ stimulated PYY secretion and the EGb $761^{(R)}$-induced PYY secretion was involved in the increase in intracellular $Ca^{2+}$ concentration and the activation of FFA4. Furthermore, in FFA4-expressing cells, EGb $761^{(R)}$ activated FFA4. These results suggest that EGb $761^{(R)}$ may affect the control of energy homeostasis via the regulation of PYY secretion and FFA4 activation.

• Animal cells and systems
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• v.16 no.4
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• pp.269-273
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• 2012

Controlling metabolism throughout life is a necessity for living creatures, and perturbation of energy balance elicits disorders such as type-2 diabetes mellitus and cardiovascular disease. $Ca^{2+}$ plays a key role in regulating energy generation. $Ca^{2+}$ homeostasis of the endoplasmic reticulum (ER) lumen is maintained through the action of $Ca^{2+}$ channels and the $Ca^{2+}$ ATPase pump. Once released from the ER, $Ca^{2+}$ is taken up by mitochondria where it facilitates energy metabolism. Mitochondrial $Ca^{2+}$ serves as a key metabolic regulator and determinant of cell fate, necrosis, and/or apoptosis. Here, we focus on $Ca^{2+}$ transport from the ER to mitochondria, and $Ca^{2+}$-dependent regulation of mitochondrial energy metabolism.

• Journal of Pharmacopuncture
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• v.14 no.2
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• pp.81-91
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• 2011

Objectives & Methods: This suggestion was attempted to be elevated the recognition of common characteristics in disease. So, we performed to analyze the correlation of common cause of disease, characteristics of human body, and medical treatment. And the results are as follows. Results: 1. The cause of disease is consist of genetic factor, aging, habit, food of not good in health, weather, environment, deficit of the physical activity, stress and so on. 2. Generally, human has common and individual weakness. Individual weakness is appeared similar to the occurrence of volcano and lapse. 3. The correlation of disease and medical treatments is possible to explain using the quotation of the law of motion made by Isaac Newton, the great physicist. 4. When the process of the medical treatment was not progressed, the prognosis is determined by the correlation of the homeostasis(H') in human body and the homeostasis(H) of disease. 5. The prognosis of disease is determined by the relationship between the energy of disease(F) and medical treatment(F'). 6. The exact diagnosis is possible to predict the treatment sequence, and the facts that homeostasis in human body and disease, relationship between the energy of disease(F) and medical treatment(F'), action and reaction are important to determine the prognosis. 7. The careful observation of improving response and worsening action of disease becomes available for exact prognosis. Conclusion: The above described contents may be useful in clinical studies, and the concrete clinical reports about this will be made afterward.

• Proceedings of the Korean Society of Applied Pharmacology
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• 2003.11a
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• pp.3-4
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• 2003

Body weight is maintained at a relatively constant level over days and months despite variability in food intake and physical activity. To achieve energy homeostasis, the hypothalamus receives information related to energy surplus or shortage from the periphery and controls food intake and energy expenditure. Leptin, an adipocyte derived hormone, is a principal mediator that signals the brain about the stored energy status. Increased leptin signaling in the brain prevents excess energy stores by suppressing food intake and increasing energy expenditure. In addition, insulin and nutrients themselves, such as glucose and free fatty acids, also regulate food intake.

• BMB Reports
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• v.48 no.12
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• pp.647-654
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• 2015

Energy homeostasis in our body system is maintained by balancing the intake and expenditure of energy. Excessive accumulation of fat by disrupting the balance system causes overweight and obesity, which are increasingly becoming global health concerns. Understanding the pathogenesis of obesity focused on studying the genes related to familial types of obesity. Recently, a rare human genetic disorder, ciliopathy, links the role for genes regulating structure and function of a cellular organelle, the primary cilium, to metabolic disorder, obesity and type II diabetes. Primary cilia are microtubule based hair-like membranous structures, lacking motility and functions such as sensing the environmental cues, and transducing extracellular signals within the cells. Interestingly, the subclass of ciliopathies, such as Bardet-Biedle and Alström syndrome, manifest obesity and type II diabetes in human and mouse model systems. Moreover, studies on genetic mouse model system indicate that more ciliary genes affect energy homeostasis through multiple regulatory steps such as central and peripheral actions of leptin and insulin. In this review, we discuss the latest findings in primary cilia and metabolic disorders, and propose the possible interaction between primary cilia and the leptin and insulin signal pathways which might enhance our understanding of the unambiguous link of a cell's antenna to obesity and type II diabetes.

• Journal of Microbiology and Biotechnology
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• v.18 no.2
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• pp.295-298
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• 2008

Creatine kinase (CK; E.C. 2.7.3.2) is an important enzyme that catalyzes the reversible transfer of a phosphoryl group from ATP to creatine in energy homeostasis. The brain-type cytosolic isoform of creatine kinase (BB-CK), which is found mainly in the brain and retina, is a key enzyme in brain energy metabolism, because high-energy phosphates are transfered through the creatine kinase/phosphocreatine shuttle system. The recombinant human BB-CK protein was overexpressed as a soluble form in Escherichia coli and crystallized at $22^{\circ}C$ using PEG 4000 as a precipitant. Native X-ray diffraction data were collected to $2.2{\AA}$ resolution using synchrotron radiation. The crystals belonged to the tetragonal space group $P4_32_12$, with cell parameters of a=b=97.963, $c=164.312{\AA},\;and\;{\alpha}={\beta}={\gamma}=90^{\circ}$. The asymmetric unit contained two molecules of CK, giving a crystal volume per protein mass $(V_m)$ of $1.80{\AA}^3\;Da^{-1}$ and a solvent content of 31.6%.

• Journal of mucopolysaccharidosis and rare diseases
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• v.2 no.2
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• pp.43-45
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• 2016

Whole body energy balance is achieved through the coordinated regulation of energy intake and energy expenditure in various tissues including liver, muscle and adipose tissues. A positive energy imbalance by excessive energy intake or insufficient energy expenditure results in obesity and related metabolic diseases. Although there have been many obesity treatment trials aimed at the reduction of energy intake, these strategies have achieved only limited success because of their associated adverse effects. Serotonin is among those traditional pharmacological targets for anti-obesity treatment because central 5-HT functions as an anorexigenic neurotransmitter in the brain. Thus, there have been many trials aimed at increasing the activity of 5-HT in the central nervous system, and some of the developed methods are already used in the clinical setting as anti-obesity drugs. However, recent studies suggest the new functions of peripheral serotonin in energy homeostasis ranging from the endocrine regulation by gut-derived serotonin to the autocrine/paracrine regulation by adipocyte-derived serotonin. Pharmacological inhibition of 5-HT synthesis leads to inhibition of lipogenesis in epididymal white adipose tissue (WAT), induction of browning in inguinal WAT and activation of adaptive thermogenesis in brown adipose tissue (BAT). Fat specific Tph1 knock-out (Tph1 FKO) mice exhibit similar phenotypes as mice with pharmacological inhibition of 5-HT synthesis, suggesting the localized effects of 5-HT in adipose tissues. In addition, Htr3a KO mice exhibit increased energy expenditure in BAT and Htr2a KO mice exhibit the decreased lipid accumulation in WAT. These data suggest the clinical significance of the peripheral serotonergic system as a new therapeutic target for anti-obesity treatment.