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Pengabdian Kepada Masyarakat

Prof. Dr. Agung Pranoto, dr.,MSc.Sp.PD-KEMD

Fakultas Kedokteran / Departemen Ilmu Penyakit Dalam

Tim Peneliti :

  1. Agung Pranoto --> Peneliti Utama

Tahun : 2009

Halaman Naskah : 1 halaman

Sumber Dana : Deprt - SMF Ilmu Penyakit Dalam FK Unair - RSUD Dr. Soetomo

Besaran Dana : 1000000

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Publikasi : Buku : Buku Kumpulan Makalah dan Abstrak, Perkembangan Endokrinologi Mutakhir dan Terintegrasi untuk Meningkatkan Pelayanan Masyarakat, mRabu 29 Juli - Sabtu 1 Agustus 2009

Kategori Penelitian : Kesehatan

Posting : 07-03-2012

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Title :

The Role Of Vitamin B In Preventing Diabetes Complication

Author : Prof. Dr. Agung Pranoto, dr.,MSc.Sp.PD-KEMD

Year : 2009

Abstact :

The Role Of Vitamin B In Preventing Diabetes Complication


Agung Pranoto

Divisi Endokrin Metabolik, Bagian SMF Penyakit Dalam

RSU Dr. Soetomo FK Unair, Surabaya, Indonesia


Type 2 Diabetes Mellitus (T2DM) is the most common of all metabolic disorders and it is a heterogeneous syndrome resulting from defects of both insulin secretion and action. The precise molecular mechanisms leading to chronic hyperglycernia are largely unknown. It is generally accepted that T2DM results form a complex interplay of genetic and environmental factors that influence a number of intermediate traits of relevance to the diabetic phenotype (e.g., ß‑cell mass, insulin secretion, insulin action, fat distribution, obesity). People with diabetes may experience many serious, long‑term complications. Some of these complications begin within months of the onset of diabetes, although most tend to develop after a few years. Most of the complications are progressive. Several pathomechanism that was discovered was increased polyol pathway flux, increased formation of advanced glycation end products (AGEs), activation of protein kinase C (PKC), increased hexosamine pathway flux, increase superoxide production by the mitochondria. Accumulation of triosephosphates arising from high cytosolic glucose concentrations in hyperglycernia is one likely or potential trigger for biochemical dysfunction leading to the development of diabetic complications. This may be prevented by disposal of excess triosephosphates via the reductive pentosephosphate pathway. This pathway is impaired in experimental and clinical diabetes by mild thiamine deficiency. The expression and activity of the :thiamine dependent enzyme, transketolase the pacemaking enzyme of the reductive pentosephosphate pathway, is consequently decreased. Correction of thiamine deficiency in experimental diabetes by high dose therapy with thiamine and the thiamine monophosphate prodrug, benfotiamine, restores disposal of triosephosphates by the reductive pentosephosphate 1~pathway in hyperglycemia. This prevented multiple mechanisms of biochemical dysfunction via ‑activation of protein kinase C,activation of the hexosamine pathway, increased glycation and oxidative stress. Consequently, the development of incipient diabetic nephropathy, neuropathy and retinopathy might be prevented. Both thiamine and Benfotiamine produced other remarkable effects in experimental diabetes: marked reversals of increased diuresis and glucosuria without change inglycernic status. High dose thiamine also corrected dyslipidernia in experimental diabetes ‑normalizing cholesterol and triglycerides.


Dysfunction of beta‑cells and impaired glucose tolerance in thiamine deficiency and suggestion of a link of impaired glucose tolerance with dietary thiamine indicates that thiamine therapy may have a future role in prevention of type 2 diabetes. More immediately, given the emerging multiple benefits of thiamine repletion, even mild thiamine deficiency in diabetes should be avoided and thiamine supplementation to high dose should be considered as adjunct nutritional therapy to prevent dyslipidemia and the development of vascular complications in clinical diabetes.

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