• Asian-Australasian Journal of Animal Sciences
• /
• v.21 no.6
• /
• pp.845-852
• /
• 2008

The goal of this study was to determine whether galanin affects the mean plasma concentrations of metabolic parameters such as thyroxine (T4), triiodothyronine (T3), growth hormone (GH), insulin, glucagon, glucose, fatty acid and urea in goats fed diets differing in energy content. Sixteen goats were randomly divided into 4 groups. Animals in groups 1 and 2 were fed 100% and animals in groups 3 and 4 were fed 50% energy content in the diet for 20 days. After 20 days, animals in groups 1 and 3 received a daily infusion of $1{\mu}g$ galanin and groups 2 and 4 received a daily infusion of $2{\mu}g$ galanin into their third ventricle for 5 days. Blood samples were collected daily from the jugular vein before infusion on day 4 until 4 days after the last infusion of galanin. Samples were assayed for plasma T3, T4, GH, insulin and glucagon concentrations by double-antibody RIA. Glucose, fatty acid and urea concentrations were also measured. Lower dietary energy intake and infusions of 1 and $2{\mu}g$ galanin significantly (p<0.01) decreased the mean plasma concentrations of T3, T4, insulin and glucose and significantly (p<0.01) increased the mean plasma concentrations of GH, glucagon, fatty acid and urea of the animals in groups 3 and 4. Different dosages of the galanin infusions did not change the plasma concentrations of the metabolic parameters in the animals fed a normal dietary energy content. The results of this experiment indicated that galanin may negatively affect T3, T4, insulin and glucose and increase GH, glucagon, fatty acid and urea in goats with negative energy balance, but not in those with positive energy balance.

• Bulletin of the Korean Chemical Society
• /
• v.34 no.1
• /
• pp.35-41
• /
• 2013

Metabolic analysis of CR6 interacting factor 1 (Crif1) deficient mouse embryonic fibroblasts with impaired oxidative phosphorylation has been carried out using LC-MS/MS and GC-MS methods. Metabolic profiles of the Crif1 deficient cells were comprehensively obtained for the first time. Loss of oxidative phosphorylation functions in mitochondria resulted in cancer-like metabolic reprogramming with consumption of majority of glucose carbon from up-regulated glycolysis to produce lactate, suppressed utilization of glucose carbon in the TCA cycle, increased amounts of amino acids. The changes in metabolic profile of the Crif1 deficient cells are most probably a consequence of metabolic reprogramming to meet the needs of energy balance and anabolic precursors in compensation for the loss of major oxidative phosphorylation functions.

• Journal of Korean Neurosurgical Society
• /
• v.42 no.6
• /
• pp.470-474
• /
• 2007

Objective : The brain is dependent on glucose as an energy source. Intricate homeostatic mechanisms have been implicated in maintaining the blood glucose concentration in the brain. The aim of this study is to find the way to identify the metabolic proteins regulating the glucose in rat hypothalamus. Methods : In this study, we analysed the secretome from rat hypothalamus in vivo. We introduced 500 nM of insulin into the rat hypothalamus. The chromatographic patterns of the secretome were identified, after which Mass Spectrometry-Mass Spectrometry (MS-MS) analysis was performed. Results : In Liquid Chromatography-Mass Spectrometry (LC-MS) analysis, 60 proteins were identified in the secretome. Among them, 8 novel proteins were unveiled and were associated with the energy metabolism of insulin signaling in mitochondria of rat hypothalamic neuron. Nineteen other proteins have unknown functions. These ligands were confirmed to be secreting from the rat hypothalmus on insulin signaling by western blotting. Conclusion : The hypothalamus is the master endocrine gland responsible for the regulation of various physiological and metabolic processes. Proteomics using LC-MS analysis offer a efficient means for generating a comprehensive analysis of hypothalamic protein expression by insulin signaling.

• Neonatal Medicine
• /
• v.17 no.2
• /
• pp.155-160
• /
• 2010

Metabolic acidosis is commonly encountered issues in the management of critically ill neonates and especially of preterm infants during early neonatal days. In extremely premature infants, low glomerular filtration rate and immaturity of renal tubules to produce new bicarbonate causes renal bicarbonate loss. Higher intake of amino acids, relatively greater contribution of protein to the energy metabolism and mineralization process in growing bones are also responsible for higher acid load in premature infant than in adult. Despite widespread use of sodium bicarbonate in the management of severe metabolic acidosis, use of sodium bicarbonate in premature infants should be restricted to a reasonable but unproven exception such as ongoing renal loss. Despite concern about the low pH value (<7.2) which can compromise cellular metabolic function, no treatment guideline has been established regarding the management of metabolic acidosis in premature infants. Appropriately powered randomized controlled trials of base therapy to treat metabolic acidosis in critically ill newborn infants are demanding.

• Korean Journal of Radiology
• /
• v.22 no.12
• /
• pp.2034-2051
• /
• 2021

Metabolic encephalopathy is a critical condition that can be challenging to diagnose. Imaging provides early clues to confirm clinical suspicions and plays an important role in the diagnosis, assessment of the response to therapy, and prognosis prediction. Diffusion-weighted imaging is a sensitive technique used to evaluate metabolic encephalopathy at an early stage. Metabolic encephalopathies often involve the deep regions of the gray matter because they have high energy requirements and are susceptible to metabolic disturbances. Understanding the imaging patterns of various metabolic encephalopathies can help narrow the differential diagnosis and improve the prognosis of patients by initiating proper treatment regimen early.

• Korean Journal of Community Nutrition
• /
• v.18 no.1
• /
• pp.77-87
• /
• 2013

This study was conducted to investigate the nutrient intakes of subjects by quartile of percent energy intake from cooked rice, consumption of cooked rice mixed with multi-grains and to evaluate rice consumption in relation to the risk of metabolic syndrome. The subjects were 5,830 males and females aged between 20~64 years based on 2007-2008 KNHNES data. Levels of percent energy intake from cooked rice were classified into 4 groups (Q1, Q2, Q3, Q4 groups: 25% of each) using data of 24-hour recall method from KNHNES. Using medical examination and questionnaire, subjects were classified according to diagnostic criteria of metabolic syndrome. The subjects with higher age, being married, lower education, lower economic level were more likely to take higher percent energy intake from cooked rice. Quartile Q3 of percent energy intake from cooked rice tended to show higher Index of Nutritional Quality (INQ) for fiber, calcium, iron, potassium and vitamin A. INQ of protein, dietary fiber, calcium, thiamin, phosphorus, potassium, riboflavin, niacin and vitamin C by consumption of cooked rice mixed with multi-grains was higher than that by consumption of cooked white rice when adjusted for age. No association with a risk for metabolic syndrome was found for quartile of percent energy intake from cooked rice or cooked rice mixed with multi-grains compared to cooked white rice after adjusting for energy, gender, age, BMI, alcohol, smoking, income and physical activity. In conclusion, consumption of over 54% energy intake from cooked rice or only cooked white rice showed relatively low INQs, but was not associated with a higher risk for metabolic syndrome.

• Korean Journal of Exercise Nutrition
• /
• v.16 no.2
• /
• pp.113-122
• /
• 2012

This study assessed the amount of energy consumed and fat deposition after endurance training in order to review the effect of 4-week endurance exercise on resting metabolic rate of a mouse during and after exercise and the effect of exercise. A total of 19 seven-week-old ICR male mice were used as the study subject. Those mice were divided into sedentary group (Sed) and trained group (Tr) after a week of environment adaption. The Tr group was trained with endurance exercise five times a week for four weeks. Weight and the amount of food intake were daily weighed and resting metabolic rate and metabolic rate after exercise were assessed before starting exercise and on the fourth week after training. Metabolic rate during exercise were measured four weeks after training. At the end of breeding period, statistically significant difference was shown in weights of trained and sedentary groups (p < 0.05). During a resting period, no significant difference was shown in oxygen intake, respiratory exchange ratio, and the amount of carbohydrate and fat oxidized. Moreover, no significant difference was shown in excess post-exercise oxygen consumption (EPOC) of an hour period after training. In contrast, the maximal oxygen uptake (VO₂ max) was approximately 11.1% higher in trained group after training compare to before. However, there was no significant difference in respiratory exchange ratio and carbohydrate and fat oxidization. During exercise, oxygen uptake, carbon dioxide production, and respiratory exchange ratio in energy metabolism during exercise showed no significant difference. However, significant difference was exhibited in the amount of fat oxidized in both groups. Summing up those results, endurance exercise could be concluded to be effective in weight control. However, weight loss is thought to be resulted from increase in fat oxidization during exercise unlike the conclusion made from previous studies where weight loss is prominently influenced by energy metabolism during a resting period and increased fat oxidation during post-exercise recovery. All experimental procedures were carried out at the Animal Experiment Research Center of Konkuk University. This study was conducted in accordance with the ethical guidelines of the Konkuk University Institutional Animal Care and Use Committee.

• Journal of Nutrition and Health
• /
• v.43 no.1
• /
• pp.5-11
• /
• 2010

We conducted comparative study on metabolizable energy content of extracts of angelica keiskei and its byproduct. Total six different groups consisting of five test groups treated with angelica keiskei and one control group were compared. Each of the five test groups were given 30% of one of whole plant, extracts, fermented of extracts, byproduct and extracts plus byproduct, respectively, mixed with AIN93M. After 3 days of adjustment period, all groups were subjected to 4 days of test period during which the amounts of feed intake and excretion were measured everyday. All feces were treated for the prevention of decomposition and changes before its energy content were measured using a bomb calorimeter. The amount of excretion was $4.8\;{\pm}\;0.3\;g$/rat/3 days in control group and 9.9-15.0 g/rat/3 days in the groups were added with extracts of angelica keiskei indicating that the angelica keiskei-treated groups produce 2-3 times more excretion. Metabolic energy of control diet was 4,133.3 kcal. This was found to be 15 to 20% higher compared with the metabolic energy content ranging from 3,117.0 kcal/kg (extracts of angelica keiskei) to 3,259.8 kcal/kg (extracts plus byproducts) angelica keiskei-treated groups. This is interpreted as the result of the decreased metabolic energy in the test diets were substituted with 30% of ngelica keiskei-treated ingredient which has low metabolic content itself. One notable finding is that the metabolic content of the group mixed with byproducts and extracts (1,763.0 kcal/kg) is 27% higher than that of extracts of angelica keiskei (1,286.8 kcal/kg) indicating that mechanical grinding increases the rate of digestion and absorption increasing, in turn, the energy content used in the body. The results of analysis of overall caloric absorption showed absorption rate in order of Whole plant < extracts < byproduct < extract plus byproduct < fermented of extract.

• Food Science and Industry
• /
• v.50 no.1
• /
• pp.26-35
• /
• 2017

Obesity is a worldwide problem that is associated with metabolic disorders. Obesity is caused by the accumulation of an abnormal amount of body fat in adipose tissue. Adipose tissue is a major metabolic organ, and it has been classified as either white adipose tissue (WAT) or brown adipose tissue (BAT). WAT and BAT are characterized by different anatomical locations, morphological structures, functions, and gene expression patterns. WAT is mainly involved in the storage and mobilization of energy in the form of triglycerides. On the other hand, BAT specializes in dissipating energy as heat through uncoupling protein-1 (UCP-1)-mediated non-shivering thermogenesis. Novel type of brown-like adipocyte within WAT called beige/brite cells was recently discovered, and this transdifferentiation process is referred to as the "browning" or "britening" of WAT. Recently, Brown fat and/or browning of WAT have been highlights as a new therapeutic target for treatment of obesity and its related metabolic disorders. Here, we describe recent advances in the study of BAT and browning of WAT, focusing on proteomic approaches.

• Biomolecules & Therapeutics
• /
• v.26 no.1
• /
• pp.69-80
• /
• 2018

Cancer cells reprogram cellular metabolism to support the malignant features of tumors, such as rapid growth and proliferation. The cancer promoting effects of metabolic reprogramming are found in many aspects: generating additional energy, providing more anabolic molecules for biosynthesis, and rebalancing cellular redox states in cancer cells. Metabolic pathways are considered the pipelines to supply metabolic cofactors of epigenetic modifiers. In this regard, cancer metabolism, whereby cellular metabolite levels are greatly altered compared to normal levels, is closely associated with cancer epigenetics, which is implicated in many stages of tumorigenesis. In this review, we provide an overview of cancer metabolism and its involvement in epigenetic modifications and suggest that the metabolic adaptation leading to epigenetic changes in cancer cells is an important non-genetic factor for tumor progression, which cooperates with genetic causes. Understanding the interaction of metabolic reprogramming with epigenetics in cancers may help to develop novel or highly improved therapeutic strategies that target cancer metabolism.