Berberine-stimulated glucose uptake in L6 myotubes involves both AMPK and p38 MAPK

Cheng, Zhe; Pang, Tao; Gu, Min; Gao, Anran; Xie, Chuan‐Ming; Li, Jing-Ya; Nan, Fa‐Jun; Li, Jingya

doi:10.1016/j.bbagen.2006.09.007

Cited by 212 publications

(159 citation statements)

References 39 publications

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“…Intraperitoneal administration of BBR into obese db/db mice reduced body weight without a significant effect on food intake ( Fig. 1, A and B), which is consistent with previous reports (5,9,16,19,38). In addition, we observed that BBR lowered the RQ ratio and increased energy expenditure (Fig.…”

Section: Bbr Alleviates Dyslipidemia and Fatty Liver In Obese Micesupporting

confidence: 81%

“…We and others (9,19,38) have reported that BBR reduces body weight, causes a significant improvement in glucose tolerance, and improves insulin action in obese and/or diabetic subjects by activating AMPK. A large body of evidence indicates that BBR enhances insulin sensitivity and reduces hyperlipidemia (5,9,16,38). Thus it is plausible to speculate that this mechanism might be applied therapeutically to treat fatty liver and hyperlipidemia.…”

mentioning

confidence: 99%

“…Berberine (BBR) is a naturally occurring structurally characterized compound present in many herbs and has a variety of pharmacological properties including glucose lowering (9,15,41) and antimicrobial activities (17). We and others (9,19,38) have reported that BBR reduces body weight, causes a significant improvement in glucose tolerance, and improves insulin action in obese and/or diabetic subjects by activating AMPK.…”

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confidence: 99%

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Berberine improves lipid dysregulation in obesity by controlling central and peripheral AMPK activity

Kim

Lee

Hun

et al. 2009

American Journal of Physiology-Endocrinology and Metabolism

209

146

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AMP-activated protein kinase (AMPK) plays an important role in regulating whole body energy homeostasis. Recently, it has been demonstrated that berberine (BBR) exerts antiobesity and antidiabetic effects in obese and diabetic rodent models through the activation of AMPK in peripheral tissues. Here we show that BBR improves lipid dysregulation and fatty liver in obese mice through central and peripheral actions. In obese db/db and ob/ob mice, BBR treatment reduced liver weight, hepatic and plasma triglyceride, and cholesterol contents. In the liver and muscle of db/db mice, BBR promoted AMPK activity and fatty acid oxidation and changed expression of genes involved in lipid metabolism. Additionally, intracerebroventricular administration of BBR decreased the level of malonyl-CoA and stimulated the expression of fatty acid oxidation genes in skeletal muscle. Together, these data suggest that BBR would improve fatty liver in obese subjects, which is probably mediated not only by peripheral AMPK activation but also by neural signaling from the central nervous system.

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Section: Bbr Alleviates Dyslipidemia and Fatty Liver In Obese Micesupporting

confidence: 81%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Berberine improves lipid dysregulation in obesity by controlling central and peripheral AMPK activity

Kim

Lee

Hun

et al. 2009

American Journal of Physiology-Endocrinology and Metabolism

209

146

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“…Thus pharmacological intervention that can reduce insulin hypersecretion and simultaneously alleviate insulin resistance is an attractive strategy to prevent beta-cell dysfunction due to their exhaustion. Berberine exerts hypoglycemic and hypolipidemic action via stimulating glucose uptake, reducing lipogenesis, and increasing energy expenditure in peripheral tissues [8,9,20]. Berberine can also decrease insulin levels in high-fat-fed rats [10].…”

Section: Discussionmentioning

confidence: 99%

“…It has been shown that berberine is a potent hypoglycemic agent with beneficial metabolic effects on peripheral tissues [6,7], which is attributed to the activation of AMP-activated protein kinase (AMPK) [8,9]. Circulating insulin levels decrease in high-fat-fed rats after berberine treatment [10], and the question remains whether this is due solely to the improvement of peripheral insulin resistance or the direct effect of berberine on islet function.…”

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confidence: 99%

Berberine inhibits glucose oxidation and insulin secretion in rat islets

et al. 2018

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Abstract. Glucose promotes insulin secretion primarily via its metabolism and the production of metabolic coupling factors in beta-cells. The activation of AMP-activated protein kinase (AMPK), an energy sensor, results in a decrease in insulin secretion from beta-cells, but its mechanism remains largely unknown. Berberine, an oral anti-diabetic drug, has been shown to activate AMPK in multiple peripheral tissues. Here, we examined the effects of berberine and AMPK activation on insulin secretion and glucose oxidation in rat islets. Our results showed that berberine inhibited glucose-stimulated insulin secretion from rat islets with AMPK activation. When glucose concentration was elevated to 25 mmol/L, the inhibitory action of berberine on insulin secretion disappeared. Furthermore, berberine significantly decreased oxygen consumption rate (OCR) and ATP production induced by high glucose in rat islets. Although adenovirus-mediated overexpression of constituentactivated AMPK markedly decreased GSIS and OCR in rat islets, the inhibition of AMPK by compound C did not reverse berberine-suppressed OCR. In addition, berberine attenuated glucose-stimulated expression of fatty acid synthase. These results indicate that berberine-mediated deceleration of glucose oxidation is tightly link to the decreased insulin secretion in islets independent of AMPK activation and inhibition of fatty acid synthesis may also contribute to the effect of berberine on insulin secretion.

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