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BBR decreased fasting blood glucose without improvement in insulin sensitivity.(A) Effects of BBR treatment on OGTT in diabetic rats. Oral glucose tolerance test (OGTT) was conducted with glucose 2 g.kg−1 body wt after 5 week BBR treatment (380 mg.kg−1 day−1) (n = 6). (B) Insulin release during the OGTT (n = 6). (C) ITT test (n = 6). The test was conducted after 8 hour fasting with insulin (0.75 U.kg−1 body wt). Nor, normal rats without obesity; Diab+Veh: Diabetic rats treated with vehicle; Diab+BBR, diabetic rats treated with BBR. # P<0.05, compared with Diab+Veh. (D) Insulin signaling. Phosphorylation of Akt (Ser473). Rats were challenged with insulin (0.75 U.kg−1, intraperitoneal injection) and liver was collected in 30 minutes. The Akt assay was performed in a Western blot. Loading control is GAPDH. (E) Expression and phosphorylation of AMPK (Thr172). # P<0.05, compared with Diab+Veh group. * P<0.05, compared with normal group (Nor).
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pone-0016556-g001: BBR decreased fasting blood glucose without improvement in insulin sensitivity.(A) Effects of BBR treatment on OGTT in diabetic rats. Oral glucose tolerance test (OGTT) was conducted with glucose 2 g.kg−1 body wt after 5 week BBR treatment (380 mg.kg−1 day−1) (n = 6). (B) Insulin release during the OGTT (n = 6). (C) ITT test (n = 6). The test was conducted after 8 hour fasting with insulin (0.75 U.kg−1 body wt). Nor, normal rats without obesity; Diab+Veh: Diabetic rats treated with vehicle; Diab+BBR, diabetic rats treated with BBR. # P<0.05, compared with Diab+Veh. (D) Insulin signaling. Phosphorylation of Akt (Ser473). Rats were challenged with insulin (0.75 U.kg−1, intraperitoneal injection) and liver was collected in 30 minutes. The Akt assay was performed in a Western blot. Loading control is GAPDH. (E) Expression and phosphorylation of AMPK (Thr172). # P<0.05, compared with Diab+Veh group. * P<0.05, compared with normal group (Nor).

Mentions: Systemic insulin sensitivity was evaluated by fasting glucose, GTT and ITT. In the GTT test, the BBR group exhibited lower blood glucose than the un-treated control at the basal level (Fig. 1A). After oral glucose challenge, the untreated group had little increase in blood glucose. The blood glucose only increased modestly by the glucose challenge. However, the BBR group exhibited a dramatic increase in blood glucose at 30 and 60 minutes. The glucose reached to the same level as the untreated group at 90 and 120 minutes. In the test, blood insulin was monitored at each time point to determine the pancreatic beta cell function. The BBR group and untreated group had identical basal insulin. However, the BBR group exhibited a significantly higher insulin level than the untreated group between 15–60 minutes after the glucose challenge (Fig. 1B). In the ITT test, both the BBR group and untreated group exhibited similar change in percentage of blood glucose at 60–90 minutes, but the BBR group had less response than the untreated group during 15–45 minutes (Fig. 1C), suggesting a delayed response to insulin in the BBR group. Those data demonstrate that BBR reduces fasting blood glucose without altering blood insulin in the basal condition, suggesting an increase in systemic insulin sensitivity by HOMA-IR. Though GTT and ITT results do not support that systemic insulin sensitivity was improved by BBR, the results may not be definitive. Hyperinsulinemic-euglycemic clamping is required to determine insulin sensitivity.

Berberine Improves Glucose Metabolism in Diabetic Rats by Inhibition of Hepatic Gluconeogenesis

Xia X, Yan J, Shen Y, Tang K, Yin J, Zhang Y, Yang D, Liang H, Ye J, Weng J - PLoS ONE (2011)

Bottom Line: We observed that BBR decreased fasting glucose significantly.In cultured hepatocytes, BBR inhibited oxygen consumption and reduced intracellular adenosine triphosphate (ATP) level.The gluconeogenic inhibition is likely a result of mitochondria inhibition by BBR.

Affiliation: Department of Endocrinology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.

ABSTRACT
Berberine (BBR) is a compound originally identified in a Chinese herbal medicine Huanglian (Coptis chinensis French). It improves glucose metabolism in type 2 diabetic patients. The mechanisms involve in activation of adenosine monophosphate activated protein kinase (AMPK) and improvement of insulin sensitivity. However, it is not clear if BBR reduces blood glucose through other mechanism. In this study, we addressed this issue by examining liver response to BBR in diabetic rats, in which hyperglycemia was induced in Sprague-Dawley rats by high fat diet. We observed that BBR decreased fasting glucose significantly. Gluconeogenic genes, Phosphoenolpyruvate carboxykinase (PEPCK) and Glucose-6-phosphatase (G6Pase), were decreased in liver by BBR. Hepatic steatosis was also reduced by BBR and expression of fatty acid synthase (FAS) was inhibited in liver. Activities of transcription factors including Forkhead transcription factor O1 (FoxO1), sterol regulatory element-binding protein 1c (SREBP1) and carbohydrate responsive element-binding protein (ChREBP) were decreased. Insulin signaling pathway was not altered in the liver. In cultured hepatocytes, BBR inhibited oxygen consumption and reduced intracellular adenosine triphosphate (ATP) level. The data suggest that BBR improves fasting blood glucose by direct inhibition of gluconeogenesis in liver. This activity is not dependent on insulin action. The gluconeogenic inhibition is likely a result of mitochondria inhibition by BBR. The observation supports that BBR improves glucose metabolism through an insulin-independent pathway.

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