Thiamin deficiency impairs endotoxin-induced increases in hepatic glucose output.
Am J Clin Nutr
; 59(5): 1045-9, 1994 May.
Article
en En
| MEDLINE
| ID: mdl-8172089
We addressed the role of thiamin, a cofactor for several enzymes involved in glucose metabolism, in the glucose metabolic response to endotoxin. Characterized by hyperglycemia, increased hepatic glucose production exceeding elevated rates of whole-body glucose utilization, this response is mediated by hormones and cytokines and is dependent on the immune and nutritional status of the host. We hypothesized that a thiamin-deficient state would impair the metabolic response to endotoxin. Rats were fed a thiamin-deficient or control diet for 6 wk before in vivo assessment of glucose kinetics. In control rats, Escherichia coli endotoxin increased the rate of glucose appearance (+76%), disappearance (+70%), and metabolic clearance (+50%). Thiamin deficiency resulted in increased plasma glucose (18%) and lactate (3- to 4-fold) as well as in a 30% decrease in insulin and an increase in glucagon (2.6-fold) and corticosterone (3.6-fold). Thiamin deficiency inhibited the endotoxin-induced hyperglycemia and the rise in hepatic glucose production, glucose utilization, and metabolic clearance rate.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Deficiencia de Tiamina
/
Endotoxinas
/
Glucosa
/
Hígado
Límite:
Animals
Idioma:
En
Revista:
Am J Clin Nutr
Año:
1994
Tipo del documento:
Article
Pais de publicación:
Estados Unidos