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Model of Streptozotocin-nicotinamide Induced Type 2 Diabetes: a Comparative Review.
Rais, Nadeem; Ved, Akash; Ahmad, Rizwan; Parveen, Kehkashan; Gautam, Girendra Kumar; Bari, Darakhshan Gazala; Shukla, Karuna S; Gaur, Ravi; Singh, Akhand Pratap.
Afiliación
  • Rais N; Department of Pharmacy, Bhagwant University, Ajmer, Rajasthan-305004, India.
  • Ved A; Goel Institute of Pharmaceutical Sciences, Lucknow, Uttar Pradesh-226028, India.
  • Ahmad R; Department of Pharmacy, Vivek College of Technical Education, Bijnor, Uttar Pradesh-246701, India.
  • Parveen K; Interdisciplinary Biotechnology Unit, Aligarh Muslim University, Aligarh, Uttar Pradesh-202002, India.
  • Gautam GK; Shri Ram College of Pharmacy, Muzaffarnagar, Uttar Pradesh-251001, India.
  • Bari DG; Department of Pharmacy, Bhagwant University, Ajmer, Rajasthan-305004, India.
  • Shukla KS; Goel Institute of Pharmaceutical Sciences, Lucknow, Uttar Pradesh-226028, India.
  • Gaur R; All India Institute of Medical Sciences, Jodhpur, Rajasthan, India.
  • Singh AP; Maharshi University of Information Technology, Lucknow, India.
Curr Diabetes Rev ; 18(8): e171121198001, 2022.
Article en En | MEDLINE | ID: mdl-34789130
The aim of the present study was to review the streptozotocin-nicotinamide (STZ-NA) diabetes model. Type 2 diabetes is more prevalent (90-95%) in adults than type 1. Experimentally- induced diabetes models may be established by chemicals, viral agents, insulin antibodies, surgery, etc. The most advisable and prompt method to induce diabetes is using chemicals, and STZ and alloxan are widely used chemicals. STZ has proven to be a better diabetogenic agent than alloxan because alloxan has many drawbacks, as it induces only type 1 diabetes, has a high mortality rate in rats, and causes ketosis in animals. Moreover, it has lesser selectivity towards ß-cells, and the diabetes-induced is reversible. STZ can be used to induce both type 1 and type 2 diabetes. It is noted that the genotoxic behavior of STZ in animals is accomplished through a reduction of nicotinamide adenine dinucleotide (NAD+) in pancreatic ß-cells via the GLUT2 (Glucose transporter 2), which can cause cellular damage by DNA (Deoxyribonucleic acid) strand breaks that lead to cell death. NA is a biochemical precursor of NAD+, and it is a poly-ADP-ribose-polymerase-1 (PARP- 1) inhibitor. NAD+ is an important redox reaction co-enzyme for the production of adenosine triphosphate (ATP) and many other metabolic pathways. Extreme DNA damage contributes to the over-activation of PARP-1, loss of cellular resources, and necrotic cells death. Some studies have expressed that NA can protect pancreatic ß-cells against the severe cytotoxicity of STZ. The review concluded that the STZ-NA model is dependent on the competency of NA to attain partial protection against the ß-cytotoxic essence of STZ to induce type-2 diabetes.
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Texto completo: 1 Base de datos: MEDLINE Asunto principal: Diabetes Mellitus Experimental / Diabetes Mellitus Tipo 2 Límite: Animals / Humans Idioma: En Revista: Curr Diabetes Rev Asunto de la revista: ENDOCRINOLOGIA Año: 2022 Tipo del documento: Article País de afiliación: India

Texto completo: 1 Base de datos: MEDLINE Asunto principal: Diabetes Mellitus Experimental / Diabetes Mellitus Tipo 2 Límite: Animals / Humans Idioma: En Revista: Curr Diabetes Rev Asunto de la revista: ENDOCRINOLOGIA Año: 2022 Tipo del documento: Article País de afiliación: India