Ranitidine induces inhibition and structural changes in sucrase

Minai-Tehrani, Dariush; Ghaffari, Mina; Sobhani-Damavandifar, Zahra; Minoui, Saeed; Alavi, S. Kh.; Osmani, Rahele; Ahmadi, Shiva

doi:10.3109/14756366.2011.601414

Cited by 6 publications

(5 citation statements)

References 13 publications

(18 reference statements)

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“…For example, N -butyldeoxynojirimycin (miglustat) that is used for treatment of lysosomal storage diseases can heavily inhibit SI and thus result in gastrointestinal symptoms in the majority of the patients [ 12 ]. Codeine as a pain medication and ranitidine with antihistamine effect can also inhibit sucrase activity in the intestine [ 13 , 14 ]. Furthermore, several herbal folk remedies, especially those with polyphenolic components, also exert an inhibitory effect on SI [ 15 ].…”

Section: Secondary Deficiencies Of Si Activitymentioning

confidence: 99%

The multiple roles of sucrase-isomaltase in the intestinal physiology

Gericke¹,

Amiri²,

Naim³

2016

Mol Cell Pediatr

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Osmotic diarrhea and abdominal pain in humans are oftentimes associated with carbohydrate malabsorption in the small intestine due to loss of function of microvillar disaccharidases. Disaccharidases are crucial for the digestion and the subsequent absorption of carbohydrates. This review focuses on sucrase-isomaltase as the most abundant intestinal disaccharidase and the primary or induced pathological conditions that affect its physiological function. Congenital defects are primary factors which directly influence the transport and function of sucrase-isomaltase in a healthy epithelium. Based on the mutation type and the pattern of inheritance, a mutation in the sucrase-isomaltase gene may exert a variety of symptoms ranging from mild to severe. However, structure and function of wild type sucrase-isomaltase can be also affected by secondary factors which influence its structure and function either specifically via certain inhibitors and therapeutic agents or generally as a part of intestinal pathogenesis, for example in the inflammatory responses. Diagnosis of sucrase-isomaltase deficiency and discriminating it from other gastrointestinal intolerances can be latent in the patients because of common symptoms observed in all of these cases.Here, we summarize the disorders that implicate the digestive function of sucrase-isomaltase as well as the diagnostic and therapeutic strategies utilized to restore normal intestinal function.

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Section: Secondary Deficiencies Of Si Activitymentioning

confidence: 99%

The multiple roles of sucrase-isomaltase in the intestinal physiology

Gericke¹,

Amiri²,

Naim³

2016

Mol Cell Pediatr

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“…There are two forms of mixed inhibition: non-and anticompetitive and non-and competitive. Metformin exhibited binding to both the active site of the enzyme and the enzyme−substrate complex, in a similar manner to drugs like ranitidine 26 and methocarbamol. 27 Table 1 shows that when the metformin concentration increases, the apparent rate constant decreases, while the apparent Michaelis−Menten constant of invertase increases, indicating a mixed inhibition manner existed.…”

Section: T H Imentioning

confidence: 91%

Metformin-Induced Invertase Unfolding: Enzyme Kinetics and Activity Regulation

Tang,

Ye,

et al. 2024

J. Agric. Food Chem.

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The effects of metformin on invertase activity and its inhibition on sucrose digestion were studied. The rapid unfolding kinetics of invertases, followed a two-state model with an inactive intermediate formation. The dynamic interaction between metformin and invertase caused the secondary structure of the enzyme to become less β-sheet, more α-helix, and random coiling oriented, which weakened the binding force between enzyme and its substrate. Metformin acted as a chaotrope and disrupted the hydrogen bonds of water, which facilitated the unfolding of invertase. However, some sugar alcohols, which promoted the Hbond formation of water, could repair the secondary structure of metformin-denatured invertase and therefore regulate the enzyme activity. This research enriches our understanding of the mechanism of enzyme unfolding induced by guanidine compounds. Moreover, because metformin and sugar substitutes are of concern to diabetes, this research also provides useful information for understanding the activity of the digestive enzyme that coexists with metformin and sugar alcohols.

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“…нестероидные противовоспалительные препараты [16,17] кодеин [18] ранитидин [19] антибиотики [20][21][22][23] Аутоиммунные заболевания: целиакия [24][25][26] язвенный колит [27] болезнь Крона [28] Вирусы иммунодефицита человека [29][30][31] Кишечные инфекции [32,33] Ишемия кишки [34] Хронические стрессы [35] Дефицит железа [35] Дефицит витамина А [35] Существует большое количество сообщений о фармакологических средствах, применяемых для лечения ожирения и диабета, основанных на подавлении активности дисахаридаз в СОТК [36]. Некоторые из них, например N-бутилдеоксиноиримицин (миглустат), используются для лечения болезней Гоше и Ниманна-Пика и вызывают диарею у большинства пациентов, так как подавляют активность мембранных ферментов [37].…”

Section: причины источникиunclassified

“…Некоторые из них, например N-бутилдеоксиноиримицин (миглустат), используются для лечения болезней Гоше и Ниманна-Пика и вызывают диарею у большинства пациентов, так как подавляют активность мембранных ферментов [37]. Кодеин и ранитидин обладают ингибирующим влиянием на активность сахаразы в СОТК [18,19].…”

Section: причины источникиunclassified

Enteropathy with impaired membrane digestion and the prospects for cytoprotective therapy

Парфенов

Иванович²,

Akhmadullina

et al. 2021

Terapevticheskii arkhiv

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The article describes enteropathy with impaired membrane digestion (EIMD) as a new nosological form. The main clinical manifestation of EIMD is the poor tolerance of food products, in particular carbohydrates and a decrease in the activity of membrane enzymes, in particular, carbohydrates, in the mucous membrane of the small intestine. The cause of the disease can be acute intestinal infections, viruses, drugs and other agents that damage the small intestine. The pathophysiology, clinical picture and diagnosis of EIMD are described. The basis of therapy is rebamipide, which has the ability to reduce the symptoms of carbohydrate intolerance and increase the activity of disaccharidases.

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Ranitidine induces inhibition and structural changes in sucrase

Cited by 6 publications

References 13 publications

The multiple roles of sucrase-isomaltase in the intestinal physiology

The multiple roles of sucrase-isomaltase in the intestinal physiology

Metformin-Induced Invertase Unfolding: Enzyme Kinetics and Activity Regulation

Enteropathy with impaired membrane digestion and the prospects for cytoprotective therapy

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