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Article citations


Molina, P.E., et al. (1994) Thiamin Deficiency Impairs Endotoxin-Induced Increases in Hepatic Glucose Output. American Journal of Clinical Nutrition, 59, 1045-1049.

has been cited by the following article:

  • TITLE: Effects of 17β-Estradiol on Dopamine D2 Receptors in Thiamine-Deficient Female Rats: Consequences on Sucrose, Alcohol, Water Intakes and Body Weight

    AUTHORS: Seydou Silué, Abdoulaye Bâ

    KEYWORDS: Thiamine Deficiency, 17β-Estradiol, D2 Receptors, Sucrose, Alcohol Intakes, Body Weight

    JOURNAL NAME: Journal of Biosciences and Medicines, Vol.7 No.11, November 1, 2019

    ABSTRACT: Our previous studies showed that 17β-estradiol (E2) modulated dopamine D2 receptor in regulating body weight set-point. The aim of this study was to understand whether thiamine deficiency influenced the E2 modulation on dopamine D2 receptors, using bromocriptine mesylate (BR) and sulpiride (SUL) as selective central dopamine-D2 receptors agonist and antagonist respectively. We studied the E2-dopamine D2 receptors interferences in a 10-day thiamine-deficient female rats for which consumptions of water, sugar, alcohol and food were daily-recorded and their consequences on body weights assessed. Our results showed that the volume of water daily ingested doubled in thiamine-deficient female rats (OXT), while sugar and alcohol consumptions collapsed with decreased weight and food consumption. On the one hand, thiamine potentiated D2/BR activity (bromocriptine-activated D2 receptors) to induce sugar intake and inhibited the same D2/BR receptors to induce water intake. On the other hand, thiamine promoted D2/SUL receptors (sulpiride-inhibited D2 receptors) for enhanced alcohol intake, increased food consumption and weight gain. Taking together, thiamine modulated the actions of 17β-estradiol on both D2/BR and D2/SUL receptors activities.