• Journal of Microbiology and Biotechnology
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• v.19 no.10
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• pp.1109-1121
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• 2009

In an attempt to discover novel biomarker proteins in type 2 diabetes prognosis, we investigated the influence of hypoglycemic extracellular polysaccharides (EPS) obtained from the macrofungus Tremella fuciformis on the differential levels of plasma proteins in ob/ob mice using two-dimensional gel electrophoresis (2-DE). The 2-DE analysis demonstrated that 92 spots from about 900 visualized spots were differentially regulated, of which 40 spots were identified as principal diabetes-associated proteins. By comparing control with EPS-fed mice, we found that at least six proteins were significantly altered in ob/ob mice, including Apo A-I, IV, C-III, E, retinol-binding protein 4, and transferrin, and their levels were interestingly normalized after EPS treatment. Western blot analysis revealed that the altered levels of the two regulatory molecules highlighted in diabetes and obesity (e.g., resistin and adiponectin) were also normalized in response to EPS. The Mouse Diabetes PCR Array profiles showed that the expression of 84 genes related to the onset, development, and progression of diabetes were significantly downregulated in liver, adipocyte, and muscle of ob/ob mice. EPS might act as a potent regulator of gene expression for a wide variety of genes in ob/ob mice, particularly in obesity, insulin resistance, and complications from diabetes mellitus.

• Journal of Nutrition and Health
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• v.36 no.10
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• pp.981-989
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• 2003

The hypoglycemic effects of four edible plants (Angelicae tenuissimae (A. ten.), Pleurospermum kamtschaticum (P. kam.), Adenophora remotiflora (A. rem.) and Zanthoxylum schinifolium (Z. sch.)) in streptozotocin (STZ) -induced diabetic rats were investigated. Sprague-Dawley male rats weighing 190-230 g were induced diabetes mellitus by the STZ injection (45 mg/kg) into the tail vein and were divided into six groups ; normal, STZ-control and four edible plant groups (A. ten., P kam., A. rem. and Z. sch. groups). Normal and STZ-control groups were fed a AIN-93 diet and four groups of STZ-induced diabetic rats were fed one of each experimental diets containing 10％ of the edible plant powder for 4 weeks. Diabetic rats showed the lower weight gain compared to the normal rats. In experimental groups except P. kam., AST activities were close to normal. A. ten. group were lowered ALT activities slightly. The plasma glucose levels of the diabetic experimental groups were significantly decreased at 4th week. The plasma insulin levels in diabetic experimental groups were not significantly different compared to the STZ-control group. The liver glycogen levels in STZ injected rats were significantly lower in compared to the normal rats. However no significant differences were found in response experimental plants intake in diabetic rats. The muscle glycogen were not significantly different among all the groups.

• Journal of Microbiology and Biotechnology
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• v.18 no.12
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• pp.1895-1902
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• 2008

Adipose tissue is an important endocrine organ involved in the control of whole body energy homeostasis and insulin sensitivity. Considering the increased incidence of obesity and obesity-related disorders, including diabetes, it is important to understand thoroughly the process of adipocyte differentiation and its control. Therefore, we performed a differential proteome mapping strategy using two-dimensional gel electrophoresis combined with peptide mass fingerprinting to identify intracellular proteins that are differentially expressed during adipose conversion of 3T3-L1 pre-adipocytes in response to an adipogenic cocktail. In the current study, we identified 46 differentially expressed proteins, 6 of which have not been addressed previously in 3T3-L1 cell differentiation. Notably, we found that phosphoribosyl pyrophosphate synthetase (PRPS), a regulator of cell proliferation, was preferentially expressed in pre-adipocytes than in fully differentiated adipocytes. In conclusion, our results provide valuable information for further understanding of the adipogenic process.

• Journal of Community Nutrition
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• v.8 no.2
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• pp.76-89
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• 2006

By improving body composition, such as fat, lean body mass and total body weight, an exercise program can be an effective treatment of obesity. The effects of exercise on obesity have been confirmed via various approaches such as type, intensity, duration, frequency, and combination with diet. Combined exercise and diet is the most efficient strategy for weight loss, and exercise alone could improve metabolism irrespective of weight loss. In addition, physical activity, including exercise, is emphasized to avoid a 'yo-yo' phenomenon. Exercise increases lipolysis stimulated by such factors as catecholamine, growth hormone (GH), and hormone sensitive lipase (HSL). Moreover, changes in insulin and cortisol through exercise affect adipose tissue, which is known as not only an energy storage locale, but also as an endocrine organ. Adipocytokines secreted by adipose tissue respond to signals that modulate metabolism and inflammation. Exercise has generally shown positive effects on adipocytokines, and these effects increase in conjunction with a hypocaloric diet. However, a long duration and a high intensity of exercise could induce an inflammatory response. This review summarizes the effects of exercise on obesity treatment, which contributes to the exercise and nutritional fields, particularly of community nutritionists. (J Community Nutrition 8(2): 76-89, 2006)

• Journal of the Korean Society of Food Science and Nutrition
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• v.21 no.6
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• pp.627-632
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• 1992

The effect of dietary pectin in the upper gastrointestinal transit rate was studied. Rats fed fiber-free diet or 10% pectin diet were offered 51-$CrCl_3,$ a transit marker. The movement of 51-Cr dose through the gastrointestinal tract was measured at intervals from 20 minutes to 6 hours after dosing. pectin significantly increased gastric emptying rate upto 3 hours after dosing. Pectin also increased small intestinal transit rate from 3 hours to 4 hours after dosing. The results suggest that delayed gastric emptying is not likely the important aspect of the mechanism by which pectin could flatten the post-prandial response of serum glucose and insulin.

• Biomedical Science Letters
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• v.22 no.3
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• pp.107-114
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• 2016

Maintenance of fasting blood glucose levels is important for glucose homeostasis. Disruption of feedback mechanisms are a major reason for elevations of glucose level in blood, which is a risk factor for type 2 diabetes mellitus that is mainly caused by malfunction of pancreatic beta-cell and insulin. The fasting blood glucose level has been known to be influenced by genetic and environmental factors. Mitochondria have many functions for cell survival and death: glucose metabolism, fatty acid oxidation, ATP generation, reactive oxygen species (ROS) metabolism, calcium handling, and apoptosis regulation. In addition to these functions, mitochondria change their morphology dynamically in response to multiple signals resulting in fusion and fission. In this study, we aimed to examine association between fasting blood glucose levels and variants of the genes that are reported to have functions in mitochondrial dynamics, fusion and fission, using a cohort study. A total 416 SNPs from 36 mitochondrial dynamics genes were selected to analyze the quantitative association with fasting glucose level. Among the 416 SNPs, 4 SNPs of PRKACB, 13 SNPs of PPP3CA, 6 SNPs of PARK2, and 3 SNPs of GDAP1 were significantly associated. In this study, we were able to confirm an association of mitochondrial dynamics genes with glucose levels. To our knowledge our study is the first to identify specific SNPs related to fasting blood glucose level.

• BMB Reports
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• v.54 no.9
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• pp.451-457
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• 2021

Over the last decades, research has focused on the role of pleckstrin homology (PH) domain leucine-rich repeat protein phosphatases (PHLPPs) in regulating cellular signaling via PI3K/Akt inhibition. The PKB/Akt signaling imbalances are associated with a variety of illnesses, including various types of cancer, inflammatory response, insulin resistance, and diabetes, demonstrating the relevance of PHLPPs in the prevention of diseases. Furthermore, identification of novel substrates of PHLPPs unveils their role as a critical mediator in various cellular processes. Recently, researchers have explored the increasing complexity of signaling networks involving PHLPPs whereby relevant information of PHLPPs in metabolic diseases was obtained. In this review, we discuss the current knowledge of PHLPPs on the well-known substrates and metabolic regulation, especially in liver, pancreatic beta cell, adipose tissue, and skeletal muscle in relation with the stated diseases. Understanding the context-dependent functions of PHLPPs can lead to a promising treatment strategy for several kinds of metabolic diseases.

• Archives of Pharmacal Research
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• v.23 no.4
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• pp.267-282
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• 2000

Cytochrome P45O (CYP) 2E1 catalyzes the metabolism of a wide variety of therapeutic agents, procarcinogens, and low molecular weight solvents. CYP2E1-catalyzed metabolism may cause toxicity or DNA damage through the production of toxic metabolites, oxygen radicals, and lipid peroxidation. CYP2E1 also plays a role in the metabolism of endogenous compounds including fatty acids and ketone bodies. The regulation of CYP2E1 expression is complex, and involves transcriptional, post-transcriptional, translational, and post-translational mechanisms. CYP2E1 is transcriptionally activated in the first few hours after birth. Xenobiotic inducers elevate CYP2E1 protein levels through both increased translational efficiency and stabilization of the protein from degradation, which appears to occur primarily through ubiquitination and proteasomal degradation. CYP2E1 mRNA and protein levels are altered in response to pathophysiologic conditions by hormones including insulin, glucagon, growth hormone, and leptin, and growth factors including epidermal growth factor and hepatocyte growth factor, providing evidence that CYP2E1 expression is under tight homeostatic control.

• Archives of Obesity and Metabolism
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• v.2 no.2
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• pp.45-53
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• 2023

Despite the emergence of obesity as a significant public health concern, artificial sweeteners have made their way into various food products due to the perception, that they serve as substitutes for sugar. Artificial sweeteners are used to supposedly achieve weight management and health improvement. However, their efficacy and safety remain debatable. Commonly used artificial sweeteners include aspartame, acesulfame potassium, saccharin, and sucralose. This article discusses the effects of artificial sweetener consumption on weight loss, appetite regulation, blood glucose control, and gut microbiota. Research findings, concerning the consumption of artificial sweeteners and their association with body weight, have shown inconsistencies between randomized controlled trials and cohort studies. Studies, comparing artificial sweeteners to sugar, have reported no significant differences in satiety. Although artificial sweeteners have no calories, they can affect blood sugar levels through the cephalic phase insulin response. A recent study suggested that artificial sweeteners influenced the occurrence of diabetes. Due to limitations in the study design, excluding diabetes-influencing factors was not feasible. The evidence showed that artificial sweeteners harbored potential health risks, necessitating further investigation. According to recent studies, the consumption of artificial sweeteners was associated with gut microbiota changes and individual blood sugar responses. It is important to note that artificial sweeteners cannot be considered safe alternatives to sugar, and further research is required.

• Asian-Australasian Journal of Animal Sciences
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• v.18 no.5
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• pp.747-754
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• 2005

Nutritional regulation of gene expression associated with growth and feeding behavior in avian species can become an important technique to improve poultry production according to the supply of nutrients in the diet. Insulin-like growth factor-I (IGF-I) found in chickens has been characterized to be a 70 amino acid polypeptide and plays an important role in growth and metabolism. Although it is been well known that IGF-I is highly associated with embryonic development and post-hatching growth, changes in the distribution of IGF-I gene expression throughout early- to late-embryogenesis have not been studied so far. We revealed that the developmental pattern of IGF-I gene expression during embryogenesis differed among various tissues. No bands of IGF-I mRNA were detected in embryonic liver at 7 days of incubation, and thereafter the amount of hepatic IGF-I mRNA was increased from 14 to 20 days of incubation. In eyes, a peak in IGF-I mRNA levels occurred at mid-embryogenesis, but by contrast, IGF-I mRNA was barely detectable in the heart throughout all incubation periods. In the muscle, no significant difference in IGF-I gene expression was observed during different stages of embryogenesis. After hatching, hepatic IGF-I gene expression as well as plasma IGF-I concentration increases rapidly with age, reaches a peak before sexual maturity, and then declines. The IGF-I gene expression is very sensitive to changes in nutritional conditions. Food-restriction and fasting decreased hepatic IGF-I gene expression and refeeding restored IGF-I gene expression to the level of fed chickens. Dietary protein is also a very strong factor in changing hepatic IGF-I gene expression. Refeeding with dietary protein alone successfully restored hepatic IGF-I gene expression of fasted chickens to the level of fed controls. In most circumstances, IGF-I makes a complex with specific high-affinity IGF-binding proteins (IGFBPs). So far, four different IGFBPs have been identified in avian species and the major IGFBP in chicken plasma has been reported to be IGFBP-2. We studied the relationship between nutritional status and IGFBP-2 gene expression in various tissues of young chickens. In the liver of fed chickens, almost no IGFBP-2 mRNA was detected. However, fasting markedly increased hepatic IGFBP-2 gene expression, and the level was reduced after refeeding. In the gizzard of well-fed young chickens, IGFBP-2 gene expression was detected and fasting significantly elevated gizzard IGFBP-2 mRNA levels to about double that of fed controls. After refeeding, gizzard IGFBP-2 gene expression decreased similar to hepatic IGFBP-2 gene expression. In the brain, IGFBP-2 mRNA was observed in fed chickens and had significantly decreased by fasting. In the kidney, IGFBP-2 gene expression was observed but not influenced by fasting and refeeding. Recently, we have demonstrated in vivo that gizzard and hepatic IGFBP-2 gene expression in fasted chickens was rapidly reduced by intravenous administration of insulin, as indicated that in young chickens the reduction in gizzard and hepatic IGFBP-2 gene expression in vivo stimulated by malnutrition may be, in part, regulated by means of the increase in plasma insulin concentration via an insulin-response element. The influence of dietary protein source (isolated soybean protein vs. casein) and the supplementation of essential amino acids on gizzard IGFBP-2 gene expression was examined. In both soybean protein and casein diet groups, the deficiency of essential amino acids stimulated chickens to increase gizzard IGFBP-2 gene expression. Although amino acid supplementation of a soybean protein diet significantly decreased gizzard IGFBP-2 mRNA levels, a similar reduction was not observed in chickens fed a casein diet supplemented with amino acids. This overview of nutritional regulation of IGF-I and IGFBP-2 gene expression in young chickens would serve for the establishment of the supply of nutrients to diets to improve poultry production.