Regulation of muscle fructose 2,6-bisphosphate levels by sulfonylureas.

Matsuda, Masafumi; Kaku, Kohei; Kaneko, Takeshi

doi:10.1507/endocrj1954.33.913

Cited by 9 publications

(3 citation statements)

References 18 publications

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“…With regard to chlorpropamide, others (Mongeet al 1986) have shown increases in the levels of fructose-2,6-bisphosphate, the important regulator of glycolysis and gluconeogenesis (Hers and Hue 1983) in chlorpropamide-treated hepatocytes. Similar findings have been observed following the addition of tolbutamide to rat liver (Matsutani, Kaku and Kaneko 1984) and mouse hind limb (Matsuda, Kaku and Kaneko 1986) perfusions. Decreases in cAMP levels have also been associated with chlorpropamide-induced inhibition of hepatic gluconeogenesis (Blumenthal 1977;Blumenthaland Whitmer 1979).…”

Section: Discussionsupporting

confidence: 83%

Postreceptor Regulation of Insulin Action in Primary Cultures of Rat Hepatocytes by Oral Hypoglycemic Agents: Effects of Linogliride and Chlorpropamide

Sj²,

Jm³

1989

Horm Metab Res

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We have previously demonstrated the ability of the sulfonylurea tolazamide to potentiate insulin action in primary cultures of hepatocytes prepared from normal and streptozotocin-diabetic rats. To determine whether the pirogliride derivative linogliride, a non-sulfonylurea orally effective hypoglycemic agent, can potentiate insulin action, we evaluated the ability of linogliride to affect insulin-stimulated lipogenesis in primary cultures of hepatocytes prepared from normal rats. In addition, we also evaluated the ability of the sulfonylurea chlorpropamide to affect insulin-stimulated lipogenesis in the same in vitro system. The exposure of hepatocytes for 18 h to either linogliride (100 ug/ml) or chlorpropamide (175 ug/ml) resulted in dose-dependent (0.1 to 100 nM insulin) increases in insulin-stimulated lipogenesis, although the effects of chlorpropamide are approximately two times those of linogliride. This increase in insulin responsiveness was not associated with any change in insulin sensitivity (ED50) or insulin binding. The results provide evidence for an extra-pancreatic effect of linogliride and chlorpropamide in the liver and indicate that these structurally unrelated oral hypoglycemic agents enhance insulin responsiveness through postbinding mechanisms.

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Section: Discussionsupporting

confidence: 83%

Postreceptor Regulation of Insulin Action in Primary Cultures of Rat Hepatocytes by Oral Hypoglycemic Agents: Effects of Linogliride and Chlorpropamide

Sj²,

Jm³

1989

Horm Metab Res

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“…Thus, extrapancreatic action such as stimulating liver and muscle fructose-2,6-bisphosphate formation may be involved in the effect of both glibenclamide and extracts used in this study rather than insulin secretion. In fact, it has been known that the extrapancreatic action of glibenclamide has an important role to inhibit glucose production by liver and improve carbohydrate metabolism in diabetes [34, 35], and increases glucose disposal by stabilizing GLUT1 protein at the plasma membrane of muscle [36]. Subsequently, we found that crude extract of A. indicum acts as a PPAR γ ligand.…”

Section: Discussionmentioning

confidence: 78%

Antidiabetic Activities of Abutilon indicum (L.) Sweet Are Mediated by Enhancement of Adipocyte Differentiation and Activation of the GLUT1 Promoter

Krisanapun

Lee

Peungvicha

et al. 2011

Evidence-Based Complementary and Alternative Medicine

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Abutilon indicum (L.) Sweet is an Asian phytomedicine traditionally used to treat several disorders, including diabetes mellitus. However, molecular mechanisms supporting the antidiabetic effect of A. indicum L. remain unknown. The aim of this study was to evaluate whether extract of A. indicum L. improves insulin sensitivity. First, we observed the antidiabetic activity of aqueous extract of the entire plant (leaves, twigs and roots) of A. indicum L. on postprandial plasma glucose in diabetic rats. The subsequent experiments revealed that butanol fractions of the extract bind to PPARγ and activate 3T3-L1 differentiation. To measure glucose uptake enhanced by insulin-like activity, we used rat diaphragm incubated with various concentrations of the crude extract and found that the extract enhances glucose consumption in the incubated solution. Our data also indicate that the crude extract and the fractions (water and butanol) did not affect the activity of kinases involved in Akt and GSK-3β pathways; however, the reporter assay showed that the crude extract could activate glucose transporter 1 (GLUT1) promoter activity. These results suggest that the extract from A. indicum L. may be beneficial for reducing insulin resistance through its potency in regulating adipocyte differentiation through PPARγ agonist activity, and increasing glucose utilization via GLUT1.

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“…Nowadays, fructose-2,6-bisphosphate is thought to be a potential activator of PFK, a key enzyme of glycolysis [7]. Also, it is known that the fructose-2,6-bisphosphate level in muscles is regulated by insulin and tolbutamide [18,19]. Although we did not examine the fructose-2,6-bisphosphate level in muscles in this experiment, the fructose-2,6-bisphosphate level should be low in mild diabetic rats.…”

Section: Discussionmentioning

confidence: 99%

Ketone Body Utilization and Its Metabolic Effect in Resting Muscles of Normal and Streptozotocin-Diabetic Rats.

et al. 1991

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Abstract. By using an in situ rat hindquarter perfusion, we evaluated ketone body utilization and its metabolic effects in the resting muscle of 24 h fasted normal and streptozotocin (STZ)-diabetic rats . Under the perfusion with ketone body-supplementation(1 mM each of acetoacetic acid (AcAc) and 3-hydroxybutyric acid (3-OHB)), the AcAc and 3-OHB uptake of STZ-diabetic rats was significantly (P<0.05) smaller than that of normal rats. This might be explained by the low enzyme activity of 3-oxoacid CoA transferase demonstrated in the hindlimb muscles of STZ-diabetic rats and this reduced ketone body uptake would be one of the causes of the development of diabetic ketoacidosis . The glucose uptake and the phosphofructokinase (PFK) activity of normal rats were significantly (P<0 .05) higher than those of STZ-diabetic rats. In both normal and STZ-diabetic rats, the glucose utilization and PFK activity of the muscles in the ketone body-supplemented condition were significantly (P<0 .05) lower than those in the non-supplemented condition. This inhibition of glucose utilization by ketone bodies should be due to the mechanism by which the oxidation of ketone bodies inhibits PFK in the muscle .

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Regulation of muscle fructose 2,6-bisphosphate levels by sulfonylureas.

Abstract: We examined the effect of sulfonylureas on the level of fructose 2,

Cited by 9 publications

References 18 publications

Postreceptor Regulation of Insulin Action in Primary Cultures of Rat Hepatocytes by Oral Hypoglycemic Agents: Effects of Linogliride and Chlorpropamide

Postreceptor Regulation of Insulin Action in Primary Cultures of Rat Hepatocytes by Oral Hypoglycemic Agents: Effects of Linogliride and Chlorpropamide

Antidiabetic Activities of Abutilon indicum (L.) Sweet Are Mediated by Enhancement of Adipocyte Differentiation and Activation of the GLUT1 Promoter

Ketone Body Utilization and Its Metabolic Effect in Resting Muscles of Normal and Streptozotocin-Diabetic Rats.

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