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Showing 1 to 12 of 263 entries
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Decreased expression of hepatic glucokinase in type 2 diabetes.

Molecular metabolism

Haeusler RA, Camastra S, Astiarraga B, Nannipieri M, Anselmino M, Ferrannini E.
PMID: 25737948
Mol Metab. 2014 Dec 18;4(3):222-6. doi: 10.1016/j.molmet.2014.12.007. eCollection 2015 Mar.

BACKGROUND/OBJECTIVES: Increased endogenous glucose production is a hallmark of type 2 diabetes. Evidence from animal models has suggested that a likely cause of this is increased mRNA expression of glucose 6-phosphatase and phosphoenolpyruvate carboxykinase (encoded by G6PC, PCK1 and...

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Haeusler RA, Camastra S, Astiarraga B, et al. Decreased expression of hepatic glucokinase in type 2 diabetes. Mol Metab. 2014;4(3):222-6doi: 10.1016/j.molmet.2014.12.007.
Haeusler, R. A., Camastra, S., Astiarraga, B., Nannipieri, M., Anselmino, M., & Ferrannini, E. (2015). Decreased expression of hepatic glucokinase in type 2 diabetes. Molecular metabolism, 4(3), 222-6. https://doi.org/10.1016/j.molmet.2014.12.007
Haeusler, Rebecca A, et al. "Decreased expression of hepatic glucokinase in type 2 diabetes." Molecular metabolism vol. 4,3 (2015): 222-6. doi: https://doi.org/10.1016/j.molmet.2014.12.007
Haeusler RA, Camastra S, Astiarraga B, Nannipieri M, Anselmino M, Ferrannini E. Decreased expression of hepatic glucokinase in type 2 diabetes. Mol Metab. 2014 Dec 18;4(3):222-6. doi: 10.1016/j.molmet.2014.12.007. eCollection 2015 Mar. PMID: 25737948; PMCID: PMC4338311.
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A gut-brain neural circuit controlled by intestinal gluconeogenesis is crucial in metabolic health.

Molecular metabolism

Soty M, Penhoat A, Amigo-Correig M, Vinera J, Sardella A, Vullin-Bouilloux F, Zitoun C, Houberdon I, Mithieux G.
PMID: 25685698
Mol Metab. 2014 Dec 26;4(2):106-17. doi: 10.1016/j.molmet.2014.12.009. eCollection 2015 Feb.

OBJECTIVES: Certain nutrients positively regulate energy homeostasis via intestinal gluconeogenesis (IGN). The objective of this study was to evaluate the impact of a deficient IGN in glucose control independently of nutritional environment.METHODS: We used mice deficient in the intestine...

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Soty M, Penhoat A, Amigo-Correig M, et al. A gut-brain neural circuit controlled by intestinal gluconeogenesis is crucial in metabolic health. Mol Metab. 2014;4(2):106-17doi: 10.1016/j.molmet.2014.12.009.
Soty, M., Penhoat, A., Amigo-Correig, M., Vinera, J., Sardella, A., Vullin-Bouilloux, F., Zitoun, C., Houberdon, I., & Mithieux, G. (2015). A gut-brain neural circuit controlled by intestinal gluconeogenesis is crucial in metabolic health. Molecular metabolism, 4(2), 106-17. https://doi.org/10.1016/j.molmet.2014.12.009
Soty, Maud, et al. "A gut-brain neural circuit controlled by intestinal gluconeogenesis is crucial in metabolic health." Molecular metabolism vol. 4,2 (2015): 106-17. doi: https://doi.org/10.1016/j.molmet.2014.12.009
Soty M, Penhoat A, Amigo-Correig M, Vinera J, Sardella A, Vullin-Bouilloux F, Zitoun C, Houberdon I, Mithieux G. A gut-brain neural circuit controlled by intestinal gluconeogenesis is crucial in metabolic health. Mol Metab. 2014 Dec 26;4(2):106-17. doi: 10.1016/j.molmet.2014.12.009. eCollection 2015 Feb. PMID: 25685698; PMCID: PMC4314540.
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Lack of hepcidin expression attenuates steatosis and causes fibrosis in the liver.

World journal of hepatology

Lu S, Bennett RG, Kharbanda KK, Harrison-Findik DD.
PMID: 26855692
World J Hepatol. 2016 Feb 08;8(4):211-25. doi: 10.4254/wjh.v8.i4.211.

AIM: To investigate the role of key iron-regulatory protein, hepcidin in non-alcoholic fatty liver disease (NAFLD).METHODS: Hepcidin (Hamp1) knockout and floxed control mice were administered a high fat and high sucrose (HFS) or a regular control diet for 3...

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Lu S, Bennett RG, Kharbanda KK, et al. Lack of hepcidin expression attenuates steatosis and causes fibrosis in the liver. World J Hepatol. 2016;8(4):211-25doi: 10.4254/wjh.v8.i4.211.
Lu, S., Bennett, R. G., Kharbanda, K. K., & Harrison-Findik, D. D. (2016). Lack of hepcidin expression attenuates steatosis and causes fibrosis in the liver. World journal of hepatology, 8(4), 211-25. https://doi.org/10.4254/wjh.v8.i4.211
Lu, Sizhao, et al. "Lack of hepcidin expression attenuates steatosis and causes fibrosis in the liver." World journal of hepatology vol. 8,4 (2016): 211-25. doi: https://doi.org/10.4254/wjh.v8.i4.211
Lu S, Bennett RG, Kharbanda KK, Harrison-Findik DD. Lack of hepcidin expression attenuates steatosis and causes fibrosis in the liver. World J Hepatol. 2016 Feb 08;8(4):211-25. doi: 10.4254/wjh.v8.i4.211. PMID: 26855692; PMCID: PMC4733464.
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Resveratrol improves glycemic control in insulin-treated diabetic rats: participation of the hepatic territory.

Nutrition & metabolism

Yonamine CY, Pinheiro-Machado E, Michalani ML, Freitas HS, Okamoto MM, Corrêa-Giannella ML, Machado UF.
PMID: 27366200
Nutr Metab (Lond). 2016 Jun 29;13:44. doi: 10.1186/s12986-016-0103-0. eCollection 2016.

BACKGROUND: Resveratrol is a natural polyphenol that has been proposed to improve glycemic control in diabetes, by mechanisms that involve improvement in insulin secretion and activity. In type 1 diabetes (T1D), in which insulin therapy is obligatory, resveratrol treatment...

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Yonamine CY, Pinheiro-Machado E, Michalani ML, et al. Resveratrol improves glycemic control in insulin-treated diabetic rats: participation of the hepatic territory. Nutr Metab (Lond). 2016;13:44doi: 10.1186/s12986-016-0103-0.
Yonamine, C. Y., Pinheiro-Machado, E., Michalani, M. L., Freitas, H. S., Okamoto, M. M., Corrêa-Giannella, M. L., & Machado, U. F. (2016). Resveratrol improves glycemic control in insulin-treated diabetic rats: participation of the hepatic territory. Nutrition & metabolism, 1344. https://doi.org/10.1186/s12986-016-0103-0
Yonamine, Caio Yogi, et al. "Resveratrol improves glycemic control in insulin-treated diabetic rats: participation of the hepatic territory." Nutrition & metabolism vol. 13 (2016): 44. doi: https://doi.org/10.1186/s12986-016-0103-0
Yonamine CY, Pinheiro-Machado E, Michalani ML, Freitas HS, Okamoto MM, Corrêa-Giannella ML, Machado UF. Resveratrol improves glycemic control in insulin-treated diabetic rats: participation of the hepatic territory. Nutr Metab (Lond). 2016 Jun 29;13:44. doi: 10.1186/s12986-016-0103-0. eCollection 2016. PMID: 27366200; PMCID: PMC4928352.
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Antcin K, a Triterpenoid Compound from Antrodia camphorata, Displays Antidiabetic and Antihyperlipidemic Effects via Glucose Transporter 4 and AMP-Activated Protein Kinase Phosphorylation in Muscles.

Evidence-based complementary and alternative medicine : eCAM

Kuo YH, Lin CH, Shih CC, Yang CS.
PMID: 27242912
Evid Based Complement Alternat Med. 2016;2016:4867092. doi: 10.1155/2016/4867092. Epub 2016 May 08.

The purpose of this study was to screen firstly the potential effects of antcin K (AnK), the main constituent of the fruiting body of Antrodia camphorata, in vitro and further evaluate the activities and mechanisms in high-fat-diet- (HFD-) induced...

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Kuo YH, Lin CH, Shih CC, et al. Antcin K, a Triterpenoid Compound from Antrodia camphorata, Displays Antidiabetic and Antihyperlipidemic Effects via Glucose Transporter 4 and AMP-Activated Protein Kinase Phosphorylation in Muscles. Evid Based Complement Alternat Med. 2016;2016:4867092doi: 10.1155/2016/4867092.
Kuo, Y. H., Lin, C. H., Shih, C. C., & Yang, C. S. (2016). Antcin K, a Triterpenoid Compound from Antrodia camphorata, Displays Antidiabetic and Antihyperlipidemic Effects via Glucose Transporter 4 and AMP-Activated Protein Kinase Phosphorylation in Muscles. Evidence-based complementary and alternative medicine : eCAM, 20164867092. https://doi.org/10.1155/2016/4867092
Kuo, Yueh-Hsiung, et al. "Antcin K, a Triterpenoid Compound from Antrodia camphorata, Displays Antidiabetic and Antihyperlipidemic Effects via Glucose Transporter 4 and AMP-Activated Protein Kinase Phosphorylation in Muscles." Evidence-based complementary and alternative medicine : eCAM vol. 2016 (2016): 4867092. doi: https://doi.org/10.1155/2016/4867092
Kuo YH, Lin CH, Shih CC, Yang CS. Antcin K, a Triterpenoid Compound from Antrodia camphorata, Displays Antidiabetic and Antihyperlipidemic Effects via Glucose Transporter 4 and AMP-Activated Protein Kinase Phosphorylation in Muscles. Evid Based Complement Alternat Med. 2016;2016:4867092. doi: 10.1155/2016/4867092. Epub 2016 May 08. PMID: 27242912; PMCID: PMC4875994.
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Anti-diabetic effect of purple corn extract on C57BL/KsJ db/db mice.

Nutrition research and practice

Huang B, Wang Z, Park JH, Ryu OH, Choi MK, Lee JY, Kang YH, Lim SS.
PMID: 25671064
Nutr Res Pract. 2015 Feb;9(1):22-9. doi: 10.4162/nrp.2015.9.1.22. Epub 2015 Jan 28.

BACKGROUND/OBJECTIVES: Recently, anthocyanins have been reported to have various biological activities. Furthermore, anthocyanin-rich purple corn extract (PCE) ameliorated insulin resistance and reduced diabetes-associated mesanginal fibrosis and inflammation, suggesting that it may have benefits for the prevention of diabetes and...

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Huang B, Wang Z, Park JH, et al. Anti-diabetic effect of purple corn extract on C57BL/KsJ db/db mice. Nutr Res Pract. 2015;9(1):22-9doi: 10.4162/nrp.2015.9.1.22.
Huang, B., Wang, Z., Park, J. H., Ryu, O. H., Choi, M. K., Lee, J. Y., Kang, Y. H., & Lim, S. S. (2015). Anti-diabetic effect of purple corn extract on C57BL/KsJ db/db mice. Nutrition research and practice, 9(1), 22-9. https://doi.org/10.4162/nrp.2015.9.1.22
Huang, Bo, et al. "Anti-diabetic effect of purple corn extract on C57BL/KsJ db/db mice." Nutrition research and practice vol. 9,1 (2015): 22-9. doi: https://doi.org/10.4162/nrp.2015.9.1.22
Huang B, Wang Z, Park JH, Ryu OH, Choi MK, Lee JY, Kang YH, Lim SS. Anti-diabetic effect of purple corn extract on C57BL/KsJ db/db mice. Nutr Res Pract. 2015 Feb;9(1):22-9. doi: 10.4162/nrp.2015.9.1.22. Epub 2015 Jan 28. PMID: 25671064; PMCID: PMC4317475.
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Marker Enzymes of Rat Chemical Hepatocarcinogenesis in Human Liver Tumors.

Pathology oncology research : POR

Kovalszky, Schaff Z, Lapis K, Jeney A.
PMID: 11173585
Pathol Oncol Res. 1996;2(1):56-58. doi: 10.1007/BF02893950.

Reduced glucose-6-phosphatase, increased GGT activity and reduction of cytochrome P-450 content are considered to be markers of chemical hepatocarcinogenesis in rats. The significance of these changes were studied in certain human liver lesions; adenoma, focal nodular hyperplasia and hepatocellular...

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Kovalszky, Schaff Z, Lapis K, et al. Marker Enzymes of Rat Chemical Hepatocarcinogenesis in Human Liver Tumors. Pathol Oncol Res. 1996;2(1):56-58doi: 10.1007/BF02893950.
Kovalszky, Schaff, Z., Lapis, K., & Jeney, A. (1996). Marker Enzymes of Rat Chemical Hepatocarcinogenesis in Human Liver Tumors. Pathology oncology research : POR, 2(1), 56-58. https://doi.org/10.1007/BF02893950
Kovalszky, Ilona, et al. "Marker Enzymes of Rat Chemical Hepatocarcinogenesis in Human Liver Tumors." Pathology oncology research : POR vol. 2,1 (1996): 56-58. doi: https://doi.org/10.1007/BF02893950
Kovalszky, Schaff Z, Lapis K, Jeney A. Marker Enzymes of Rat Chemical Hepatocarcinogenesis in Human Liver Tumors. Pathol Oncol Res. 1996;2(1):56-58. doi: 10.1007/BF02893950. PMID: 11173585.
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Reactivation by phospholipids of CCl(4) inhibited microsomal glucose-6-phosphatase.

FEBS letters

Kaschnitz R, Mittermayer K.
PMID: 11947007
FEBS Lett. 1969 May;3(3):202-204. doi: 10.1016/0014-5793(69)80135-3.

No abstract available.

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Kaschnitz R, Mittermayer K. Reactivation by phospholipids of CCl(4) inhibited microsomal glucose-6-phosphatase. FEBS Lett. 1969;3(3):202-204doi: 10.1016/0014-5793(69)80135-3.
Kaschnitz, R., & Mittermayer, K. (1969). Reactivation by phospholipids of CCl(4) inhibited microsomal glucose-6-phosphatase. FEBS letters, 3(3), 202-204. https://doi.org/10.1016/0014-5793(69)80135-3
Kaschnitz, R, and Mittermayer, K. "Reactivation by phospholipids of CCl(4) inhibited microsomal glucose-6-phosphatase." FEBS letters vol. 3,3 (1969): 202-204. doi: https://doi.org/10.1016/0014-5793(69)80135-3
Kaschnitz R, Mittermayer K. Reactivation by phospholipids of CCl(4) inhibited microsomal glucose-6-phosphatase. FEBS Lett. 1969 May;3(3):202-204. doi: 10.1016/0014-5793(69)80135-3. PMID: 11947007.
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Glucose-6-phosphatase in tubular endoplasmic reticulum of hepatocytes.

Science (New York, N.Y.)

Rosen SI, Kelly GW, Peters VB.
PMID: 17775162
Science. 1966 Apr 15;152(3720):352-4. doi: 10.1126/science.152.3720.352.

The histochemical localization of glucose-6-phosphatase activity in neonatal mouse liver was studied under electron microscopy. The activity was demonstrated in the tubular endoplasmic reticulum, which pervades the glycogen areas of the cell during glycogenolysis. Activity was also demonstrated in...

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Rosen SI, Kelly GW, Peters VB. Glucose-6-phosphatase in tubular endoplasmic reticulum of hepatocytes. Science. 1966;152(3720):352-4doi: 10.1126/science.152.3720.352.
Rosen, S. I., Kelly, G. W., & Peters, V. B. (1966). Glucose-6-phosphatase in tubular endoplasmic reticulum of hepatocytes. Science (New York, N.Y.), 152(3720), 352-4. https://doi.org/10.1126/science.152.3720.352
Rosen, S I, et al. "Glucose-6-phosphatase in tubular endoplasmic reticulum of hepatocytes." Science (New York, N.Y.) vol. 152,3720 (1966): 352-4. doi: https://doi.org/10.1126/science.152.3720.352
Rosen SI, Kelly GW, Peters VB. Glucose-6-phosphatase in tubular endoplasmic reticulum of hepatocytes. Science. 1966 Apr 15;152(3720):352-4. doi: 10.1126/science.152.3720.352. PMID: 17775162.
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Alcoholic stem extract of Coscinium fenestratum regulates carbohydrate metabolism and improves antioxidant status in streptozotocin-nicotinamide induced diabetic rats.

Evidence-based complementary and alternative medicine : eCAM

Punitha IS, Rajendran K, Shirwaikar A, Shirwaikar A.
PMID: 16136216
Evid Based Complement Alternat Med. 2005 Sep;2(3):375-81. doi: 10.1093/ecam/neh099. Epub 2005 Jul 05.

Alcoholic extract of the stems of Coscinium fenestratum, a medicinal plant indigenous to India and Sri Lanka used in ayurveda and siddha medicine for treating diabetes, was studied for its carbohydrate metabolism effect and antioxidant status in streptozotocin-nicotinamide induced...

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Punitha IS, Rajendran K, Shirwaikar A, et al. Alcoholic stem extract of Coscinium fenestratum regulates carbohydrate metabolism and improves antioxidant status in streptozotocin-nicotinamide induced diabetic rats. Evid Based Complement Alternat Med. 2005;2(3):375-81doi: 10.1093/ecam/neh099.
Punitha, I. S., Rajendran, K., Shirwaikar, A., & Shirwaikar, A. (2005). Alcoholic stem extract of Coscinium fenestratum regulates carbohydrate metabolism and improves antioxidant status in streptozotocin-nicotinamide induced diabetic rats. Evidence-based complementary and alternative medicine : eCAM, 2(3), 375-81. https://doi.org/10.1093/ecam/neh099
Punitha, I S R, et al. "Alcoholic stem extract of Coscinium fenestratum regulates carbohydrate metabolism and improves antioxidant status in streptozotocin-nicotinamide induced diabetic rats." Evidence-based complementary and alternative medicine : eCAM vol. 2,3 (2005): 375-81. doi: https://doi.org/10.1093/ecam/neh099
Punitha IS, Rajendran K, Shirwaikar A, Shirwaikar A. Alcoholic stem extract of Coscinium fenestratum regulates carbohydrate metabolism and improves antioxidant status in streptozotocin-nicotinamide induced diabetic rats. Evid Based Complement Alternat Med. 2005 Sep;2(3):375-81. doi: 10.1093/ecam/neh099. Epub 2005 Jul 05. PMID: 16136216; PMCID: PMC1193540.
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Endoplasmic reticulum stress caused by overexpression of islet-specific glucose-6-phosphatase catalytic subunit-related protein in pancreatic Beta-cells.

The review of diabetic studies : RDS

Shameli A, Yamanouchi J, Thiessen S, Santamaria P.
PMID: 17565413
Rev Diabet Stud. 2007;4(1):25-32. doi: 10.1900/RDS.2007.4.25. Epub 2007 May 10.

The high rate of protein synthesis in beta-cells renders them susceptible to endoplasmic reticulum (ER) stress, a condition that can be aggravated by additional imbalances in ER homeostasis and could potentially contribute to the pathogenesis of type-1 and type-2...

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Shameli A, Yamanouchi J, Thiessen S, et al. Endoplasmic reticulum stress caused by overexpression of islet-specific glucose-6-phosphatase catalytic subunit-related protein in pancreatic Beta-cells. Rev Diabet Stud. 2007;4(1):25-32doi: 10.1900/RDS.2007.4.25.
Shameli, A., Yamanouchi, J., Thiessen, S., & Santamaria, P. (2007). Endoplasmic reticulum stress caused by overexpression of islet-specific glucose-6-phosphatase catalytic subunit-related protein in pancreatic Beta-cells. The review of diabetic studies : RDS, 4(1), 25-32. https://doi.org/10.1900/RDS.2007.4.25
Shameli, Afshin, et al. "Endoplasmic reticulum stress caused by overexpression of islet-specific glucose-6-phosphatase catalytic subunit-related protein in pancreatic Beta-cells." The review of diabetic studies : RDS vol. 4,1 (2007): 25-32. doi: https://doi.org/10.1900/RDS.2007.4.25
Shameli A, Yamanouchi J, Thiessen S, Santamaria P. Endoplasmic reticulum stress caused by overexpression of islet-specific glucose-6-phosphatase catalytic subunit-related protein in pancreatic Beta-cells. Rev Diabet Stud. 2007;4(1):25-32. doi: 10.1900/RDS.2007.4.25. Epub 2007 May 10. PMID: 17565413; PMCID: PMC1892522.
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THE EFFECT OF DIABETES AND FASTING ON LIVER GLUCOSE-6-PHOSPHATASE.

Proceedings of the National Academy of Sciences of the United States of America

Ashmore J, Hastings AB, Nesbett FB.
PMID: 16589537
Proc Natl Acad Sci U S A. 1954 Aug;40(8):673-8. doi: 10.1073/pnas.40.8.673.

No abstract available.

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Ashmore J, Hastings AB, Nesbett FB. THE EFFECT OF DIABETES AND FASTING ON LIVER GLUCOSE-6-PHOSPHATASE. Proc Natl Acad Sci U S A. 1954;40(8):673-8doi: 10.1073/pnas.40.8.673.
Ashmore, J., Hastings, A. B., & Nesbett, F. B. (1954). THE EFFECT OF DIABETES AND FASTING ON LIVER GLUCOSE-6-PHOSPHATASE. Proceedings of the National Academy of Sciences of the United States of America, 40(8), 673-8. https://doi.org/10.1073/pnas.40.8.673
Ashmore, J, et al. "THE EFFECT OF DIABETES AND FASTING ON LIVER GLUCOSE-6-PHOSPHATASE." Proceedings of the National Academy of Sciences of the United States of America vol. 40,8 (1954): 673-8. doi: https://doi.org/10.1073/pnas.40.8.673
Ashmore J, Hastings AB, Nesbett FB. THE EFFECT OF DIABETES AND FASTING ON LIVER GLUCOSE-6-PHOSPHATASE. Proc Natl Acad Sci U S A. 1954 Aug;40(8):673-8. doi: 10.1073/pnas.40.8.673. PMID: 16589537; PMCID: PMC534140.
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