Lansoprazole enhances the antidiabetic effect of dapagliflozin in fortified diet‐fed streptozotocin‐treated diabetic rats

Gamil, Noha M.; Fattah, Mai A. Abd El; Ahmed, Maha A.E.; Maklad, Yousreya A.; Din, Amina A. Gamal el; Eid, Nihad I.

doi:10.1002/jbt.22451

Cited by 5 publications

(8 citation statements)

References 99 publications

(116 reference statements)

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“…The increase of leptin level induces the formation of free oxygen radicals. This situation triggers hyperglycemia, adiponectin level and leads to insulin resistance [22]. In the present study, the positive effect of LDAT via PPAR and AMPK effects on insulin resistance may cause the decrease in leptin and resistin levels and the increase in adiponectin levels.…”

Section: Discussionmentioning

confidence: 50%

“…This effect may occur as a result of β cell regeneration. Because the treatment provides regeneration of β cell through activation of PPARγ and AMPK [3,8,22]. HOMA-β, an indicator of B cell functionality, was significantly higher in the low-dose albendazole treatment group from the diabetes group.…”

Section: Discussionmentioning

confidence: 98%

“…Furthermore, some benzimidazole molecules cause regeneration of pancreas β cell, and the regulation of adipose tissue [21,22,26,27]. It was emphasized that telmisartan and lansoprazole, benzimidazole derivatives, could be used as an antidiabetic in the treatment of T2D by activating PPAR [27].…”

Section: Discussionmentioning

confidence: 99%

“…It was emphasized that telmisartan and lansoprazole, benzimidazole derivatives, could be used as an antidiabetic in the treatment of T2D by activating PPAR [27]. Other benzimidazole derivatives compound 991 and lansoprazole have increased glucose transport into tissues by AMPK activation or other mechanism [22,29,30]. Metformin contributes to the anthelmentic effect of albendazole by providing AMPK activation in the larval period of Echinococcus granulosus [31].…”

Section: Discussionmentioning

confidence: 99%

“…Lansoprazole, another benzimidazole derivative, has been used for the treatment of diseases such as ulcers and esophagitis for about 27 years [18]. Although lansoprazole is not reported the direct effect on the AMPK, it regenerates and sensitizes beta cells, induces peroxisome proliferatoractivated receptor-γ (PPARγ) through incretin and the regulation of lipid metabolism, and increases the insulin synthesis and adiponectin/leptin ratio [19][20][21][22]. In addition, its high doses decrease glucose, triglyceride levels, and stimulate beta cells by increasing incretin secretion, providing β cell regeneration and neogenesis, delaying gastric emptying [19][20][21][22][23].…”

mentioning

confidence: 99%

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Potential antidiabetic activity of benzimidazole derivative albendazole and lansoprazole drugs in different doses in experimental type 2 diabetic rats

Dik¹,

Coşkun²,

Bahcivan³

et al. 2021

Turk J Med Sci

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IntroductionType 2 diabetes is defined as a chronic inflammatory metabolic disease that is characterized with the impaired insulin effect and high blood glucose level [1]. The disease has degenerative effects on many tissues and a high incidence worldwide. Although many drugs are used for the treatment of this disease, more effective treatment strategies have yet to be found [2,3].Adenosine 5′-monophosphate activated protein kinase (AMPK) is considered to be an important potential therapeutic target for the treatment of type 2 diabetes (T2D). AMPK is defined as serine/threonine protein kinase complex. The kinase consists catalytic α (α1, α2), regulatory β (β1, β2), and regulatory γ (γ1, γ2, γ3) subunits and express in each tissue [3]. Although the isoforms have been reported to have different effects and tissue-specific, the effects of isoforms have not been fully cleared. However, α1 isoform predominates in the liver and adipose tissue; whereas, α2 predominates in the brain, heart, and skeletal muscles [4]. The AMPK acts as a sensor that determines the AMP/ATP or ADP/ATP ratio. The AMPK is activated by phosphorylation of Thr-172 residue in the α subunit and increasing AMP/ATP ratio in the cell [3][4][5][6]. The activated AMPK provides the phosphorylation of key metabolic proteins that inhibits anabolic activities and increase catabolic activities [3]. The AMPK activation suppresses genes mediating gluconeogenesis and lipogenesis in the liver [7], and the activation of AMPK has been reported to increase insulin secretion from pancreatic β cells [3,8]. On the contrary, the excessive increased insulin, leptin and diacylglycerol levels and hyperglycemia, hyperlipidemia inhibit the AMPK activation [6]. Therefore, the AMPK activation increases insulin sensitivity, stimulates glycogen synthesis while inhibits glycolysis. Thus, it is an important Aim: The aim of this study is to determine the effects of different concentrations of albendazole and lansoprazole, which were benzimidazole derivatives, on endocrinologic and biochemical parameters in experimental type 2 diabetic (T2D) rats. Materials and methods:In this study, 46 male Wistar Albino rats were used. Animals were divided as healthy control (0.1 mL/rat/day saline, s.c, n = 6), diabetes control (0.1 mL/rat/day saline, s.c, n = 8), diabetes+low-dose albendazole (5 mg/kg, oral, n = 8), diabetes+highdose albendazole (10 mg/kg, oral n = 8), diabetes+low-dose lansoprazole (15 mg/kg, subcutaneous, n = 8), and diabetes+high-dose lansoprazole (30 mg/kg, subcutaneous, n = 8). All groups were treated for 8 weeks. The blood samples were analyzed by autoanalyzer and ELISA kits for biochemical and endocrinological parameters, respectively.Results: Glucose, HbA1c, triglyceride, low density cholesterol (LDL), leptin, and Homeostatic Model Assessment for insulin resistance (HOMA-IR) levels increased and insulin and HOMA-β levels decreased in the diabetic rats compared to the healthy control group. The glucose, HbA1c, and triglyceride levels were partially decreased; however, insu...

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Section: Discussionmentioning

confidence: 50%

Section: Discussionmentioning

confidence: 98%