• Proceedings of the Korea Society of Poultry Science Conference
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• 2005.11a
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• pp.8-16
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• 2005

Leptin, the product of the ob gene, is primarily produced and released from adipocytes and acts on the hypothalamus to decrease food intake and increase energy expenditure. Defect in leptin or leptin receptors results in severe metabolic syndromes such as obesity, diabetes, and hypertension Evidence suggests that leptin plays beyond a satiety factor; in fact, it is a pluripotent player In regulation of numerous body functions. Although its actions have been relatively well studied in mammals scanty data are available in birds. In this article, recent advances in understanding of the roles of leptin in chicken physiology are reviewed with the focus on the effects on food intake, lipid metabolism, development and reproduction, and stress.

• Journal of the Korea Academia-Industrial cooperation Society
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• v.17 no.6
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• pp.147-156
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• 2016

The purpose of this study was to identify the factors associated with the improvement of metabolic syndrome, and provide basic data for the health management of clients. The subjects were 280 adults who were diagnosed with metabolic syndrome in 2013, and who were examined from January 2013 to December 2014. The data were analyzed by descriptive statistics, t-test, ${\chi}^2$-test, and logistic regression analysis with SPSS WIN 18. The change rate from 3 to 2 risk factors was 60.6% among those clients whose metabolic syndrome improved. The improvement group showed a decrease in their waist circumference, systolic blood pressure, triglycerides and increase in their HDL cholesterol in 2014 compared to 2013, as well as decreased drinking, increased exercise, proper calorie, protein and carbohydrate uptake, and increased consumption of a lipid lowering agent. Exercise, calorie uptake and maintenance of an oral hypoglycemic drug influenced the improvement of the metabolic syndrome. In conclusion, it is necessary to have an intervention program including exercise enhancement and diet modification and to reinforce the health education for continuing health management.

• Tuberculosis and Respiratory Diseases
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• v.78 no.4
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• pp.436-439
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• 2015

Small cell lung cancer (SCLC), which originated from neuroendocrine tissue, can develop into paraneoplastic endocrine syndromes, such as Cushing syndrome, because of an inappropriate secretion of ectopic adrenocorticotropic hormone (ACTH). This paraneoplastic syndrome is known to be a poor prognostic factor in SCLC. The reason for poor survival may be because of a higher risk of infection associated with hypercortisolemia. Therefore, early detection and appropriate treatment for this syndrome is necessary. But the diagnosis is challenging and the source of ACTH production can be difficult to identify. We report a 69-year-old male patient who had severe hypokalemia, metabolic alkalosis, and hypertension as manifestations of an ACTH-secreting small cell carcinoma of the lung. He was treated with ketoconazole and spironolactone to control the ACTH dependent Cushing syndrome. He survived for 15 months after chemotherapy, which is unusual considering the poor outcome of the ectopic ATH syndrome associated with SCLC.

• Asian-Australasian Journal of Animal Sciences
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• v.26 no.8
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• pp.1189-1196
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• 2013

Adipose tissue development and function play a critical role in the regulation of energy balance, lipid metabolism, and the pathophysiology of metabolic syndromes. Although the effect of zinc ascorbate supplementation in diabetes or glycemic control is known in humans, the underlying mechanism is not well described. Here, we investigated the effect of a zinc-chelated vitamin C (ZnC) compound on the adipogenic differentiation of 3T3-L1 preadipocytes. Treatment with ZnC for 8 d significantly promoted adipogenesis, which was characterized by increased glycerol-3-phosphate dehydrogenase activity and intracellular lipid accumulation in 3T3-L1 cells. Meanwhile, ZnC induced a pronounced up-regulation of the expression of glucose transporter type 4 (GLUT4) and the adipocyte-specific gene adipocyte protein 2 (aP2). Analysis of mRNA and protein levels further showed that ZnC increased the sequential expression of peroxisome proliferator-activated receptor gamma ($PPAR{\gamma}$) and CCAAT/enhancer-binding protein alpha (C/$EBP{\alpha}$), the key transcription factors of adipogenesis. These results indicate that ZnC could promote adipogenesis through $PPAR{\gamma}$ and C/$EBP{\alpha}$, which act synergistically for the expression of aP2 and GLUT4, leading to the generation of insulin-responsive adipocytes and can thereby be useful as a novel therapeutic agent for the management of diabetes and related metabolic disorders.

• Transactions on Electrical and Electronic Materials
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• v.17 no.6
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• pp.375-379
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• 2016

Increasing fat tissue of obese people, increases the rate of cardiovascular disease, diabetes, metabolic syndromes and dyslipidemia. An increase in the focal tissue of pancreas is a known risk factor of these diseases. Although there exists sufficient research on the diagnosis and treatment of pancreatic cancer, studies have been done on fatty pancreas. In this study, based on ultrasound imaging and using a texture characteristic of GLCM, fatty pancreas was divided into three categories: mild, moderate and severe. We compared and analyzed the three groups was by Pancreatic ultrasonography and body characteristics, serological tests, pressure and the degree of arteriosclerosis, against normal control group. The following parameters of control and test groups were measured: WC (waist circumference),BMI (body mass index), TC (total cholesterol), TG (triglyceride), HDL-C (High-density lipoprotein cholesterol) and LDL-C (Low-density lipoprotein cholesterol), SBP (systolic blood pressure), BST (Blood Sugar Test) and aortic PWV (pulse wave velocity). We observed the values correspondingly increasing fat deposition. However, ABI (Ankle Brachial pressure index) stenosis and HDL-C levels decreased with increasing fat deposit (p <0.05); a drop in these parameters are known to be harmful to the human body. The difference in texture characteristics between normal control group and pancreatic fatty group (mild, moderate, and severe) was statistically confirmed. Ultrasound imaging of pancreatic steatosis categorized the disease as mild, moderate and severe based on the characteristic texture. In conclusion, we observed on increase in metabolic syndrome, dyslipidemia, and arteriosclerosis, proportional to the degree of pancreatic fat deposition. The escalation of these diseases was confirmed and was directly related with predictors of cardiovascular diseases.

• IMMUNE NETWORK
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• v.11 no.1
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• pp.59-67
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• 2011

Background: Insulin resistance is an integral feature of metabolic syndromes, including obesity, hyperglycemia, and hyperlipidemia. In this study, we evaluated whether the aloe component could reduce obesity-induced inflammation and the occurrence of metabolic disorders such as blood glucose and insulin resistance. Methods: Male C57BL/6 obese mice fed a high-fat diet for 54 days received a supplement of aloe formula (PAG, ALS, Aloe QDM, and Aloe QDM complex) or pioglitazone (PGZ) and were compared with unsupplemented controls (high-fat diet; HFD) or mice fed a regular diet (RD). RT-PCR and western blot analysis were used to quantify the expression of obesity-induced inflammation. Results: Aloe QDM lowered fasting blood glucose and plasma insulin compared with HFD. Obesity-induced inflammatory cytokine (IL-$1{\beta}$, -6, -12, TNF-${\alpha}$) and chemokine (CX3CL1, CCL5) mRNA and protein were decreased markedly, as was macrophage infiltration and hepatic triglycerides by Aloe QDM. At the same time, Aloe QDM decreased the mRNA and protein of $PPAR{\gamma}/LXR{\alpha}$ and $11{\beta}$-HSD1 both in the liver and WAT. Conclusion: Dietary aloe formula reduces obesity-induced glucose tolerance not only by suppressing inflammatory responses but also by inducing anti-inflammatory cytokines in the WAT and liver, both of which are important peripheral tissues affecting insulin resistance. The effect of Aloe QDM complex in the WAT and liver are related to its dual action on $PPAR{\gamma}$ and $11{\beta}$-HSD1 ression and its use as a nutritional intervention against T2D and obesity-related inflammation is suggested.

• Annals of Clinical Neurophysiology
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• v.16 no.2
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• pp.74-76
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• 2014

Foot drop is usually derived from peroneal nerve injury. Traumatic causes of peroneal nerve injury are more common than insidious causes including metabolic syndromes and mass lesions. We present a case with common peroneal neuropathy due to schwannoma, which is extremely rare. Complete excision of the mass lead to a gradual improvement of the symptoms. Schwannoma should be considered as a cause of common peroneal neuropathy.

• Journal of Life Science
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• v.30 no.10
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• pp.835-843
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• 2020

Obesity, the world's leading metabolic disease, is a serious health problem in both industrialized and developing countries. Natural substances are of great interest in preventative medicine, especially in the field of metabolic syndromes-from insulin resistance to obesity and diabetes. In the present study, we investigated the effect of A. pullulans SM-2001 Extract (Polycan^®) on the adipocyte differentiation of 3T3-L1 preadipocytes and the anti-obesity effect of 3T3-L1 adipocytes. Although β-glucan has been found to have health benefits in the regulation of the immune system and blood cholesterol levels, its role in obesity has not been fully investigated. Polycan^® suppressed lipid accumulation and glycerol-3-phosphate dehydrogenase (GPDH) activity without affecting cell viability in 3T3-L1 preadipocytes and adipocytes. Polycan^® also inhibited cellular lipid accumulation through down-regulation of transcription factors, such as PPARγ and C/EBPα, and induced dose-dependent phosphorylation of AMP-activated protein kinase (AMPK)-a cellular energy sensor-while the total AMPK protein content remained unchanged. Taken together, this shows that the activation of AMPK by Polycan^® in adipocytes plays a critical role in Polycan^®-induced inhibition of adipocyte differentiation. Our results show that Polycan^® has an anti-obesity action in vitro, suggesting a potential novel preventative agent for obesity and other metabolic diseases.

• Journal of Life Science
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• v.32 no.3
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• pp.256-262
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• 2022

Oxysterols are oxygenated metabolites of cholesterol generated by serial enzymatic reactions during bile acid synthesis. Similar to cholesterol, oxysterols move rapidly to the intracellular region and modulate various cellular processes, such as immune cell responses, lipid metabolism, and cholesterol homeostasis. Different nuclear transcription factors, such as glucocorticoid, estrogen, and liver X receptors, can be modulated by oxysterols in multiple tissues. The most abundant oxysterol, 27-hydroxycholesterol (27-OHC), is a well-known selective modulator that can either activate or suppress estrogen receptor activity in a tissue-specific manner. The contribution of 27-OHC in atherosclerosis development is apparent because a large amount of it is found in atherosclerotic plaques, accelerating the transformation of macrophages into foam cells that uptake extracellular modified lipids. According to previous studies, however, there are opposing opinions about how 27-OHC affects lipid and cholesterol metabolism in metabolic organs, including the liver and adipose tissue. In particular, the effects of 27-OHC on lipid metabolism are entirely different between in vitro and in vivo conditions, suggesting that understanding the physiology of this oxysterol requires a sophisticated approach. This review summarizes the potential effects of 27-OHC in atherosclerosis and metabolic syndromes with a special discussion of its role in metabolic tissues.

• Korean Journal of Exercise Nutrition
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• v.16 no.2
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• pp.65-71
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• 2012

Oxygen is the final acceptor of electron transport from fat and carbohydrate oxidation, which is the rate-limiting factor for cellular ATP production. Under altitude hypoxia condition, energy reliance on anaerobic glycolysis increases to compensate for the shortfall caused by reduced fatty acid oxidation [1]. Therefore, training at altitude is expected to strongly influence the human metabolic system, and has the potential to be designed as a non-pharmacological or recreational intervention regimen for correcting diabetes or related metabolic problems. However, most people cannot accommodate high altitude exposure above 4500 M due to acute mountain sickness (AMS) and insulin resistance corresponding to a increased levels of the stress hormones cortisol and catecholamine [2]. Thus, less stringent conditions were evaluated to determine whether glucose tolerance and insulin sensitivity could be improved by moderate altitude exposure (below 4000 M). In 2003, we and another group in Austria reported that short-term moderate altitude exposure plus endurance-related physical activity significantly improves glucose tolerance (not fasting glucose) in humans [3,4], which is associated with the improvement in the whole-body insulin sensitivity [5]. With daily hiking at an altitude of approximately 4000 M, glucose tolerance can still be improved but fasting glucose was slightly elevated. Individuals vary widely in their response to altitude challenge. In particular, the improvement in glucose tolerance and insulin sensitivity by prolonged altitude hiking activity is not apparent in those individuals with low baseline DHEA-S concentration [6]. In addition, hematopoietic adaptation against altitude hypoxia can also be impaired in individuals with low DHEA-S. In short-lived mammals like rodents, the DHEA-S level is barely detectable since their adrenal cortex does not appear to produce this steroid [7]. In this model, exercise training recovery under prolonged hypoxia exposure (14-15% oxygen, 8 h per day for 6 weeks) can still improve insulin sensitivity, secondary to an effective suppression of adiposity [8]. Genetically obese rats exhibit hyperinsulinemia (sign of insulin resistance) with up-regulated baseline levels of AMP-activated protein kinase and AS160 phosphorylation in skeletal muscle compared to lean rats. After prolonged hypoxia training, this abnormality can be reversed concomitant with an approximately 50% increase in GLUT4 protein expression. Additionally, prolonged moderate hypoxia training results in decreased diffusion distance of muscle fiber (reduced cross-sectional area) without affecting muscle weight. In humans, moderate hypoxia increases postprandial blood distribution towards skeletal muscle during a training recovery. This physiological response plays a role in the redistribution of fuel storage among important energy storage sites and may explain its potent effect on changing body composition. Conclusion: Prolonged moderate altitude hypoxia (rangingfrom 1700 to 2400 M), but not acute high attitude hypoxia (above 4000 M), can effectively improve insulin sensitivity and glucose tolerance for humans and antagonizes the obese phenotype in animals with a genetic defect. In humans, the magnitude of the improvementvaries widely and correlates with baseline plasma DHEA-S levels. Compared to training at sea-level, training at altitude effectively decreases fat mass in parallel with increased muscle mass. This change may be associated with increased perfusion of insulin and fuel towards skeletal muscle that favors muscle competing postprandial fuel in circulation against adipose tissues.