• Journal of the Korean Society of Food Science and Nutrition
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• v.23 no.6
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• pp.879-886
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• 1994

This study was carried out to determine, the effects of sodium alginate and cellulose on the plasma lipoportein composition and cholesterol metabolism inrats.Each experimental diet contained 105 sodium alginate and cellulose by weight, respectivley and rats were fed fro 4 weeks. The results obtained were as follows : The feeding of sodium alginate and cellulose decreased total plasma cholesterol slightly . total cholesterol of Chylomicron /VLDL- , LDL-fraction and liver were decreased significantly insodium alginate group. HDL-cholesterol was slightly increased in soidum alginate group. The feeding of sodium alginate significantly lowered plasma , Chylomicron VLDL-, LDL-fraction and liver TG concentrations compared with those fed fiber-free diet . The HMG-CoA reductase activity was not different among diet groups but the lowest activity was observed in sodium alginate group. The feeding of sodium alginate significantly increased fecal cholesterol , TG, and bile acid excretion . In summary , the ingestion of sodium alginate decreased cholesterol and TG concentrations of plasma and liver. This may be explained by the facts that fecal cholesterol, bile acid and TG level were increased significantly in sodium alginate group.

• Journal of Nutrition and Health
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• v.56 no.4
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• pp.349-360
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• 2023

Purpose: Ketogenic diets (KDs) have anti-obesity effects that may be related to glucose control and the gut microbiota. This paper hypothesizes that KD reduces body weight and changes the insulin sensitivity and gut microbiota composition in a mouse model of diet-induced obesity. Methods: In this study, C57BL/6 male mice were assigned randomly to 3 groups. The assigned diets were provided to the control and high-fat (HF) diet groups for 14 weeks. The KD group was given a HF diet for 8 weeks to induce obesity, followed by feeding the KD for the next 6 weeks. Results: After the treatment period, the KD group exhibited a 35.82% decrease in body weight gain compared to the HF group. In addition, the KD group demonstrated enhanced glucose control, as shown by the lower levels of serum fasting glucose, serum fasting insulin, and the homeostatic model assessment of insulin resistance, compared to the HF group. An analysis of the gut microbiota using 16S ribosomal RNA sequencing revealed a significant decrease in the proportion of Firmicutes when the KD was administered. In addition, feeding the KD reduced the overall alpha-diversity measures and caused a notable separation of microbial composition compared to the HF diet group. The KD also led to a decrease in the relative abundance of specific species, such as Acetatifactor_muris, Ligilactobacillus_apodemi, and Muribaculum_intestinale, compared with the HF group. These species were positively correlated with the body weight, whereas the abundant species in the KD group (Kineothrix_alysoides and Saccharofermentans_acetigenes) showed a negative correlation with body weight. Conclusion: The current study presents supporting evidence that KD reduced the body weight and altered the insulin sensitivity and gut microbiota composition in a mouse model of diet-induced obesity.

• Proceedings of the Korean Society of Embryo Transfer Conference
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• 2002.11a
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• pp.99-99
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• 2002

The hormone resistin is associated with typeII diabetes mellitus in rodent model. Resistin impairs glucose tolerance and insulin action. A new class of anti-diabetic drugs were called thiazolidinediones (TZDs) downregulates a resistin which is induced during adipocyte differentiation. But the connection between increased adiposity and resistin remains unknown. The objectives of this study was to clone a mouse resistin cDNA and to generate transgenic mice overexpressing mouse resistin gene. The 555 bp of mouse resistin was amplified from mob cDNAS by polymerase chain reaction (PCR) and cloned into pCR$\^$(R)/ 2.1 TOPO T-vector. Mouse resistin mRNA on the basis of Genbank sequence (acession no. AF323080). Then, the PCR product was cloned into pTargeT$\^$TM/ mammalian expression vector that has pCMV promoter and chimeric intron. Restriction enzyme analysis with BamH I and Not I was carried out to determine an orientation of the insert in the vector. The pCMV-mus/resistin gene was prepared from previous recombinant pTargeT$\^$TM/-mus/resistin by digestion of Bgl II, and has used for microinjection into pronuclei of one cell embryos. The microinjected embryos were transfered to pseudopregnant foster-mother. Mouse resistin expression was detected in transgenic F1 mice by Reverse Transcriptase- Polymerase Chain Reaction (RT-PCR). Resistin gene expression mouse has heavier body weight which was measured higher level of plasma glucose than that of normal mouse. And in diet-induced experiments, the abdominal fat pads were isolated from each 24h starvation and re-feeding after fasting group mice that were assessed by RT-PCR analysis. In fasting group mice, resistin expression was higher than that of re-feeding group mice. This result suggests that the resistin gene overexpressing mice may be became to obesity and be useful as an animal disease model to be diabetes mellitus caused by insulin resistance of resistin.

• The Korean Journal of Physiology and Pharmacology
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• v.16 no.5
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• pp.333-337
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• 2012

Gene expression of neuronal nitric oxide synthase (nNOS) changes in the hypothalamic paraventricular nucleus (PVN) depending on feeding conditions, which is decreased during food deprivation and restored by refeeding, and phosphorylated cAMP response element binding protein (pCREB) was suggested to play a role in its regulation. This study was conducted to examine if the fasting-induced down-regulation of the PVN-nNOS expression is restored by activation of cAMP-dependent protein kinase A (cAMP/PKA) pathway. Freely moving rats received intracerebroventricular (icv) injection of cAMP/PKA activator Sp-cAMP (40 nmol) or vehicle (sterilized saline) following 48 h of food deprivation. One hour after drug injections, rats were transcardially perfused with 4% paraformaldehyde, and the PVN tissues were processed for nNOS or pCREB immunohistochemistry. Sp-cAMP significantly increased not only nNOS but also pCREB immunoreactivities in the PVN of food deprived rats. Fastinginduced down-regulation of the PVN-nNOS was restored by 1 h after the icv Sp-cAMP. Results suggest that cAMP/PKA pathway may mediate the regulation of the PVN-nNOS expression depending on different feeding conditions.

• Korean Journal of Ichthyology
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• v.22 no.3
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• pp.147-153
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• 2010

A study was carried out to examine the effect of water temperature on daily pattern and rate of total ammonia nitrogen (TAN) excretion in juvenile Pacific cod Gadus macrocephalus (mean body weight: $36.5{\pm}0.8\;g$) under fasting and feeding conditions. Fish were acclimated over 10 days under three different water temperatures (9, 11 and $13^{\circ}C$), and transferred to TAN measuring system under each water-temperature condition. After 72 hours of starving, fasting TAN excretion was measured at each temperature. To investigate post-prandial TAN excretion, fish were hand-fed with a commercial diet containing 40.6% crude protein for 7 days, two times daily at 08:00 and 16:00 h. Water was sampled from both the inlet and outlet of the fish chamber every 2 h over a 24-h period. Both fasting and post-prandial TAN excretion increased with increased water temperatures (p<0.05). Mean fasting TAN excretion rates at 9, 11 and $13^{\circ}C$ were 9.3, 11.0 and $11.9\;mg\;TAN\;kg\;fish^{-1}\;h^{-1}$, respectively. The value of $9^{\circ}C$ was lower than those of 11 and $13^{\circ}C$ (p<0.05), but there was no significant difference between $11^{\circ}C$ and $13^{\circ}C$. Mean post-prandial TAN excretion rates at 9, 11 and $13^{\circ}C$ were 23.0, 31.6 and $45.4\;mg\;TAN\;kg\;fish^{-1}\;h^{-1}$, respectively. A peak value of post-prandial TAN excretion rate occurred after 2 h from each feeding, and the second value is always higher than the first value. Maximum post-prandial TAN excretion rate occurred after 10 h from the first feeding at $9^{\circ}C$ (mean $38.0\;mg\;TAN\;kg\;fish^{-1}\;h^{-1}$), $11^{\circ}C$ ($52.9\;mg\;TAN\;kg\;fish^{-1}\;h^{-1}$) and $13^{\circ}C$ ($77.5\;mg\;TAN\;kg\;fish^{-1}\;h^{-1}$), respectively. The TAN loss for ingested nitrogen at $9^{\circ}C$ (43.9%) was lower than those of $11^{\circ}C$ (46.4%) and $13^{\circ}C$ (48.4%). The overall results indicate that water temperature exhibits a significant effect on the nitrogen excretion of juvenile Pacific cod.

• Journal of Veterinary Clinics
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• v.17 no.2
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• pp.403-410
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• 2000

The Ultrasonographic method alas been widely applied to evaluating gastric motility with safety and reproducibility ill human medicine but few reference to its use in veterinary medicine is appeared. Therefore, in this study, the gastric motility was evaluated with ultrasonography by the cri-terion of mean cycle lime, short and lony axis and the area of pyloric antrum in dogs, fed with liquid of semisolid meals. Furthermore, the animals were evaluated for the effect of metoclopramide on the motility of pyloric antrum. Healthy 5 mongrel male dogs were fed with either 400 ml of milk a: a liquid meal or a mixed meal of 200 ml of milk with two pieces of bread as a semisolid meal. Mean cycle time of pyloric antrum of dogs was significantly delayed after feeding either of liquid and , semi- solid meals(P<0.05), alls it was returned to the fasting state at 60 min. after feeding of liquid meal and 160 min. after feeding of semisolid meal. Mean area of pyloric antrum of dogs was gradually decreased and was returned to the lasting state at 80 min. in doss fed liquid meal. but 1600 min. in dog\ulcorner fed semisolid meal. The administration of metoclopramide (1.0 mg/kg of of B.W.) accelerated the mean cycle time of pyloric antrum from 20 mill. to 60 min. after feeding of liquid meal and from 40 min. to 120 min. after feeding of semisolid meal. From this study, the ultrasonography was confirmed as a valuable diagnostic method leer evaluating the gastric motility and gastric area in dogs. It is non-invasive, safe and reproducible, and provides a method for the study of the effect of drugs and diseases states on gastric motility.

• The Journal of Internal Korean Medicine
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• v.37 no.4
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• pp.609-623
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• 2016

Objective: This study was undertaken to investigate the effects of Mori folium on insulin resistance and adipose tissue inflammation in an experimental mouse model of obesity.Methods: Obesity was induced in C57BL/6 mice by feeding them a high-fat diet. The mice were divided into four groups (n=6): a normal diet, high-fat diet, high-fat diet with 40 mg of Mori folium, and high-fat diet with 800 mg of Mori folium groups. After 13 wk, the body weights, fasting blood glucose and fasting serum insulin levels, insulin resistance (homeostatic model assessment) levels, oral glucose tolerance test levels, epididymal fat and liver weights, and gene expression of tumor necrosis factor-α, interleukin-6, and interferon-γ were measured. In addition, adipose tissue macrophages were analyzed by fluorescence-activated cell sorting.Results: Mori folium significantly reduced blood glucose levels, oral glucose tolerance levels, and liver weights. It also reduced adipose tissue macrophage numbers and tumor necrosis factor receptor-α gene expression.Conclusions: These results show that Mori folium has insulin resistance reduction and anti-inflammatory effects in an experimental mouse model of obesity.

• BMB Reports
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• v.46 no.12
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• pp.567-574
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• 2013

Liver plays a major role in maintaining glucose homeostasis in mammals. Under fasting conditions, hepatic glucose production is critical as a source of fuel to maintain the basic functions in other tissues, including skeletal muscle, red blood cells, and the brain. Fasting hormones glucagon and cortisol play major roles during the process, in part by activating the transcription of key enzyme genes in the gluconeogenesis such as phosphoenol pyruvate carboxykinase (PEPCK) and glucose 6 phosphatase catalytic subunit (G6Pase). Conversely, gluconeogenic transcription is repressed by pancreatic insulin under feeding conditions, which effectively inhibits transcriptional activator complexes by either promoting post-translational modifications or activating transcriptional inhibitors in the liver, resulting in the reduction of hepatic glucose output. The transcriptional regulatory machineries have been highlighted as targets for type 2 diabetes drugs to control glycemia, so understanding of the complex regulatory mechanisms for transcription circuits for hepatic gluconeogenesis is critical in the potential development of therapeutic tools for the treatment of this disease. In this review, the current understanding regarding the roles of two key transcriptional activators, CREB and FoxO1, in the regulation of hepatic gluconeogenic program is discussed.

• BMB Reports
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• v.42 no.9
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• pp.568-573
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• 2009

Fatty acid oxidation (FAO) defects cause abnormal lipid accumulation in various tissues, which provides an opportunity to uncover novel genes that are involved in lipid metabolism. During a gene expression study in the riboflavin deficient induced FAO disorder in the chicken, we discovered the dramatic increase in mRNA levels of an uncharacterized gene, ANKRD9. No functions have been ascribed to ANKRD9 and its orthologs, although their sequences are well conserved among vertebrates. To provide insight into the function of ANKRD9, the expression of ANKRD9 mRNA in lipidperturbed paradigms was examined. The hepatic mRNA level of ANKRD9 was repressed by thyroid hormone ($T_3$) and fasting, elevated by re-feeding upon fasting. However, ANKRD9 mRNA level is reduced in response to apoptosis. Transient transfection assay with green fluorescent protein tagged- ANKRD9 showed that this protein is localized within the cytoplasm. These findings point to the possibility that ANKRD9 is involved in intracellular lipid accumulation.

• The Korean Journal of Physiology
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• v.15 no.2
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• pp.97-101
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• 1981

The early plasma gastrin responses to single oral glucose or casein solution were studied in the same normal subjects on different days. After an overnight fast, glucose or casein solution was ingested within few minutes at the breakfast time. The plasma gastrin responses to these solutions were compared and contrasted with the concentration when the subjects received glucose solution intravenously. Results were as follows: 1) Rapid intravenous glucose infusion did not produce any changes in the plasma gastrin concentration. 2) Plasma gastrin concentration rose and peaked within 10 minutes after an oral liquid ingestion and then decreased substantially by 15 minutes, but remained slightly above fasting levels at 60 minutes. 3) There was no significant difference between the mean plasma gastrin concentrations after glucose of casein ingestion, but each fluid produced a significant increase in serum gastrin above fasting levels. 4) The subjects who produced high plasma gastrin response to glucose solution did so to casein solution. Conversely a low response to one solution reflected a low response to the other solution. 5) From the above results, authors discussed that individual responsibility rather than the sorts of meals is the factor in the determination of the magnitude of the early gastrin response.