• BMB Reports
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• v.54 no.6
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• pp.323-328
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• 2021

Periodontal diseases have been reported to have a multidirectional association with metabolic disorders. We sought to investigate the correlation between periodontitis and diabetes or fatty liver disease using HFD-fed obese mice inoculated with P. gingivalis. Body weight, alveolar bone loss, serological biochemistry, and glucose level were determined to evaluate the pathophysiology of periodontitis and diabetes. For the evaluation of fatty liver disease, hepatic nonalcoholic steatohepatitis (NASH) was assessed by scoring steatosis, inflammation, hepatocyte ballooning and the crucial signaling pathways involved in liver metabolism were analyzed. The C-reactive protein (CRP) level and NASH score in P. gingivalis-infected obese mice were significantly elevated. Particularly, the extensive lobular inflammation was observed in the liver of obese mice infected with P. gingivalis. Moreover, the expression of metabolic regulatory factors, including peroxisome proliferator-activated receptor γ (Pparγ) and the fatty acid transporter Cd36, was up-regulated in the liver of P. gingivalis-infected obese mice. However, inoculation of P. gingivalis had no significant influence on glucose homeostasis, insulin resistance, and hepatic mTOR/AMPK signaling. In conclusion, our results indicate that P. gingivalis can induce the progression of fatty liver disease in HFD-fed mice through the upregulation of CD36-PPARγ axis.

• Food Science and Preservation
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• v.22 no.6
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• pp.893-900
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• 2015

In this study, we evaluated the antidiabetic effect of a submerged culture of Ceriporia lacerata mycelium (CL01) on hematological indices, as well as protein and mRNA expression of the insulin-signaling pathway, in db/db mice. After CL01 was administrated for 4 weeks, blood glucose levels decreased consistently, and plasma insulin and c-peptide levels each decreased by roughly 55.8%, 40% of those in the negative control (p<0.05). With regard to HOMA-IR, an insulin resistance index, insulin resistance of the CL01-fed group improved over that of the negative control group by about 62% (p<0.05). In addition, we demonstrated that the protein expression levels of pIR, pAkt, pAMPK, and GLUT4 and the mRNA expression levels of Akt2, IRS1, and GLUT4 in the muscle cells of db/db mice increased in the CL01-fed group compared to the corresponding levels in the control group. These results demonstrate that CL01 affects glucose metabolism, upregulates protein and gene expression in the insulin-signaling pathway, and decreases blood glucose levels effectively by improving insulin sensitivity. More than 90% of those who suffer from type 2 diabetes are more likely to suffer from hyperinsulinemia, hypertension, obesity, and other comorbidities because of insulin resistance. Therefore, it is possible that CL01 intake could be used as a fundamental treatment for type 2 diabetes by lowering insulin resistance, and these results may prove be useful as basic evidence for further research into the mechanisms of a cure for type 2 diabetes.

• Korean Journal of Food Science and Technology
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• v.51 no.1
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• pp.81-89
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• 2019

This study was performed to confirm the influence of chlorogenic acid (CGA) and 3,5-dicaffeyolquinic acid (3,5-diCQA) intake on problems caused by high-fat diet. CGA was more effective in suppressing weight gain than 3,5-diCQA. In contrast, 3,5-diCQA was more effective in improving glucose tolerance than CGA. In the biopsy, it was confirmed that CGA inhibited visceral fat and liver fat accumulation. 3,5-diCQA also inhibited visceral fat accumulation, but 3,5-diCQA increased liver fat accumulation. The liver fat accumulation induced oxidative stress, but 3,5-diCQA reduced oxidative damage through its antioxidant activity. The increased liver fat accumulation was because a 3,5-diCQA greatly increased Akt phosphorylation and decreased AMPK phosphorylation in the liver. Consequently, CGA was effective in alleviating the problems caused by high-fat diets, while maintaining normal balance. 3,5-diCQA also showed a positive effect on problems caused by high-fat diets, but it increased liver fat accumulation and thereby had negative consequences.

• Asian-Australasian Journal of Animal Sciences
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• v.31 no.4
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• pp.548-555
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• 2018

Objective: This experiment was conducted to investigate whether asparagine (Asn) could improve liver energy status in weaning pigs when challenged with lipopolysaccharide. Methods: Forty-eight weaned pigs ($Duroc{\times}Large\;White{\times}Landrace$, $8.12{\pm}0.56kg$) were assigned to four treatments: i) CTRL, piglets received a control diet and injected with sterile 0.9% NaCl solution; ii) lipopolysaccharide challenged control (LPSCC), piglets received the same control diet and injected with Escherichia coli LPS; iii) lipopolysaccharide (LPS)+0.5% Asn, piglets received a 0.5% Asn diet and injected with LPS; and iv) LPS+1.0% Asn, piglets received a 1.0% Asn diet and injected with LPS. All piglets were fed the experimental diets for 19 d. On d 20, the pigs were injected intraperitoneally with Escherichia coli LPS at $100{\mu}g/kg$ body weights or the same volume of 0.9% NaCl solution based on the assigned treatments. Then the pigs were slaughtered at 4 h and 24 h after LPS or saline injection, and the liver samples were collected. Results: At 24 h after LPS challenge, dietary supplementation with 0.5% Asn increased ATP concentration (quadratic, p<0.05), and had a tendency to increase adenylate energy charges and reduce AMP/ATP ratio (quadratic, p<0.1) in liver. In addition, Asn increased the liver mRNA expression of pyruvate kinase, pyruvate dehydrogenase, citrate synthase, and isocitrate dehydrogenase ${\beta}$ (linear, p<0.05; quadratic, p<0.05), and had a tendency to increase the mRNA expression of hexokinase 2 (linear, p<0.1). Moreover, Asn increased liver phosphorylated AMP-activated protein kinase (pAMPK)/total AMP-activated protein kinase (tAMPK) ratio (linear, p<0.05; quadratic, p<0.05). However, at 4 h after LPS challenge, Asn supplementation had no effect on these parameters. Conclusion: The present study indicated that Asn could improve the energy metabolism in injured liver at the late stage of LPS challenge.

• Korean Journal of Exercise Nutrition
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• v.13 no.2
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• pp.93-100
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• 2009

This study was conducted to investigate the effect of exercise training on blood and metabolic variances and genes expressions in hyperlipidemic rats. Three weeks-old male rats were randomly assigned into chow (n=7), high-fat diet (HF, n=7) and HF+exercise (HF+EX, n=7) groups. Exercise training consisted of the treadmill running 5 times per week during 8 weeks (0% grade, 30 min/time for first 4 weeks and 0% grade, 60 min/time the other 4weeks). The levels of triglyceride and total -cholesterol were increased in HF diet compared with chow group, and recovered to level of chow group by exercise training. Plasma glucose and insulin concentrations increased by 40 and 50%, respectively in HF diet compared with chow diet group, and these increases returned to the level of chow group by exercise training (p<.05). Body weight and abdominal fat mass were increased by high-fat diet compared with chow diet, and recovered to level of chow group by exercise training. Long-chain fatty acid oxidation rate and AMPK protein expression was not changed by HF diet, but increased by exercise training compared with high-fat diet (p<.05). UCP3 protein expression was not changed by either high-fat diet or exercise training compared with chow group. There was high correlation between plasma triglyceride and total cholesterol concentrations(p<.01). Plasma triglyceride or total cholesterol level showed correlation with following factors; plasma insulin and glucose levels, body weight, abdominal fat weight, UCP3 protein expression and long-chain fatty acid oxidation rate. These results showed that exercise training on the treadmill recovered hyperlipidemia, hyperglycemia and hyperinsulinemia induced by high-fat diet for 8 weeks. These exercise effects may be related with decreased body weight and abdominal fat mass, and increased long-chain fatty acid oxidation rate.

• Korean Journal of Plant Resources
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• v.36 no.6
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• pp.541-548
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• 2023

In the present study, the effects of HML on lipolysis, adipocyte browning, autophagy, and proliferation were investigated. HML affected lipolysis by increasing the protein levels of ATGL and HSL, and phosphorylation levels of HSL and AMPK. Furthermore, HSL decreased the perilipin-1 levels. In addition, free glycerol content was increased by HML treatment. HML affected adipocyte browning by increasing the protein levels of UCP-1, PGC-1α, and PRDM16. In addition, HML affected autophagy by increasing the levels of LC3-I and LC3-II, and decreasing those of SQSTM1/p62. Moreover, HML affected adipocyte proliferation by suppressing the proliferation of 3T3-L1 cells due to arrest of the cell cycle via blocking the expression of β-catenin and cyclin D1. These results suggest that HML induces lipolysis, adipocyte browning, autophagy, and inhibits excessive proliferation of adipocytes.

• Korean Journal of Food Science and Technology
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• v.49 no.2
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• pp.192-202
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• 2017

In this study, factors involved in lipid and energy metabolism following treatment with ethanolic extract of the Polygonatum sibiricum rhizome (ID1216) were evaluated in high-fat diet-induced obese mice. ID1216-treated mice showed a significant reduction in weight gain compared to non-treated mice. ID1216 treatment increased the protein levels of AMP-dependent protein kinase, sirtuin1, peroxisome proliferator-activated receptor ${\gamma}$ coactivator 1-${\alpha}$ ($PGC1{\alpha}$), peroxisome proliferator-activated receptor ${\alpha}$ ($PPAR{\alpha}$) and uncoupling proteins in the adipose tissue, liver and muscle compared to vehicle treatment. Analysis of downstream signals of the sirtuin1 $PGC1{\alpha}$-$PPAR{\alpha}$ pathway showed that ID1216 regulates the expression of ${\beta}$-oxidation related genes such as acyl-CoA oxidase, carnitine palmitoyltransferase1, acyl-CoA dehydrogenase and adipocyte protein 2. In addition, ID1216 increased the expression of adipose triglyceride lipase. These results suggest that ID1216 has anti-obesity effects by regulating the genes involved thermogenesis, ${\beta}$-oxidation and lipolysis in a diet-induced obesity model.

• Korean Journal of Food Science and Technology
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• v.49 no.6
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• pp.685-692
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• 2017

Mitochondrial biogenesis-a process that leads to an increment in the number and density of mitochondria, improves physical performance and body health by enhancing exercise capacity. In the present study, we investigated the stimulatory effect of Ashitaba and red ginseng complex (ARC) on exercise capacity in L6 skeletal muscle cells and mice. In L6 skeletal muscle cells, ARC increased the mitochondrial contents and ATP production by activating AMP-activated protein kinase (AMPK), sirtuin 1 (SIRT1), and peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-$1{\alpha}$) and up-regulating the mRNA expression of nuclear respiratory factor-1 (NRF-1) and mitochondrial transcription factor A (TFAM). In the animal experiments, mice treated with ARC showed an increment in exercise capacity as compared with mice treated with Ashitaba extract or red ginseng extract alone. These studies indicate that ARC might serve as a potential natural candidate for enhancing exercise capacity by stimulation of mitochondrial biogenesis.

• Nutrition Research and Practice
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• v.12 no.6
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• pp.494-502
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• 2018

BACKGROUND/OBJECTIVES: Reducing the number of adipocytes by inducing apoptosis of mature adipocytes as well as suppressing differentiation of preadipocytes plays an important role in preventing obesity. This study examines the anti-adipogenic and pro-apoptotic effect of red pepper seed water extract (RPS) prepared at $4^{\circ}C$ (RPS4) in 3T3-L1 cells. MATERIALS/METHODS: Effect of RPS4 or its fractions on lipid accumulation was determined in 3T3-L1 cells using oil red O (ORO) staining. The expressions of AMP-activated protein kinase (AMPK) and adipogenic associated proteins [peroxisome proliferator-activated receptor-${\gamma}$ ($PPAR-{\gamma}$), CCAAT/enhancer-binding proteins ${\alpha}$ (C/EBP ${\alpha}$), sterol regulatory element binding protein-1c (SREBP-1c), fatty acid synthase (FAS), and acetyl-CoA carboxylase (ACC)] were measured in 3T3-L1 cells treated with RPS4. Apoptosis and the expression of Akt and Bcl-2 family proteins [B-cell lymphoma 2 (Bcl-2), Bcl-2-associated death promoter (Bad), Bcl-2 like protein 4 (Bax), Bal-2 homologous antagonist/killer (Bak)] were measured in mature 3T3-L1 cells treated with RPS4. RESULTS: Treatment of RPS4 ($0-75{\mu}g/mL$) or its fractions ($0-50{\mu}g/mL$) for 24 h did not have an apparent cytotoxicity on pre and mature 3T3-L1 cells. RPS4 significantly suppressed differentiation and cellular lipid accumulation by increasing the phosphorylation of AMPK and reducing the expression of $PPAR-{\gamma}$, C/EBP ${\alpha}$, SREBP-1c, FAS, and ACC. In addition, all fractions except ethyl acetate fraction significantly suppressed cellular lipid accumulation. RPS4 induced the apoptosis of mature adipocytes by hypophosphorylating Akt, increasing the expression of the pro-apoptotic proteins, Bak, Bax, and Bad, and reducing the expression of the anti-apoptotic proteins, Bcl-2 and p-Bad. CONCLUSIONS: These finding suggest that RPS4 can reduce the numbers as well as the size of adipocytes and might useful for preventing and treating obesity.

• The Korea Journal of Herbology
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• v.34 no.6
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• pp.79-89
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• 2019

Objective : This study investigated the anti-diabetic effects of DM1, a herbal mixture with Atractylodis Rhizoma, Anemarrhenae Rhizoma, and Cinnamomi Cortex in high fat diet (HFD)-induced diabetic mice and the mechanism in C2C12 mouse skeletal muscle cells. Methods : The C57B/6 mice were fed high fat for 12 weeks, and then administrated DM1 extract (500 mg/kg, p.o.) for 4 weeks. The changes of body weight, calorie and water intakes, fasting blood glucose levels and the serum levels of glucose, insulin, triglyceride, HDL-cholesterol, AST and ALT were measured in mice. The histological changes of liver and pancreas tissues were also observed by H&E stain. C2C12 myoblasts were differentiated into myotubes and then treated with DM1 extract (0.5, 1, and 2 mg/㎖) for 24 hr. The expression of myosin heavy chain (MHC), PGC1α, Sirt1 and NRF1, and the AMPK phosphorylation were determined in the myotubes by western blot, respectively. Results : The DM1 extract administration significantly decreased the calorie and water intakes, glucose, triglyceride, AST and ALT levels and increased insulin and HDL-cholesterol in HFD-induced diabetic mice. DM1 extract inhibited lipid accumulation in liver tissue and improved glucose tolerance. In C2C12 myotubes, DM1 treatment increased the expression of MHC, PGC1α, Sirt-1, NRF-1 and the AMPK phosphorylation. Conclusion : In our results indicate that DM1 can improve diabetic symptoms by decreasing the obesity, glucose tolerance and fatty liver in HFD-induced diabetic mice, and responsible mechanism is might be related with energy enhancement.