Thiamin deficiency impairs endotoxin-induced increases in hepatic glucose output

Patricia E. Molina, Khalil A. Yousef, Rita M. Smith, Patrick G. Tepper, Charles H. Lang, Naji N. Abumrad

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)1045-1049
Number of pages5
JournalAmerican Journal of Clinical Nutrition
Volume59
Issue number5
DOIs
StatePublished - Jan 1 1994

Fingerprint

Thiamine Deficiency
Endotoxins
Glucose
Liver
Thiamine
Hyperglycemia
Metabolic Clearance Rate
Coenzymes
Corticosterone
Glucagon
Nutritional Status
Lactic Acid
Hormones
Insulin
Cytokines
Diet

All Science Journal Classification (ASJC) codes

  • Medicine (miscellaneous)
  • Nutrition and Dietetics

Cite this

Molina, Patricia E. ; Yousef, Khalil A. ; Smith, Rita M. ; Tepper, Patrick G. ; Lang, Charles H. ; Abumrad, Naji N. / Thiamin deficiency impairs endotoxin-induced increases in hepatic glucose output. In: American Journal of Clinical Nutrition. 1994 ; Vol. 59, No. 5. pp. 1045-1049.
@article{db59dbc4670d4eceb7a787b3e57a6f8d,
title = "Thiamin deficiency impairs endotoxin-induced increases in hepatic glucose output",
abstract = "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.",
author = "Molina, {Patricia E.} and Yousef, {Khalil A.} and Smith, {Rita M.} and Tepper, {Patrick G.} and Lang, {Charles H.} and Abumrad, {Naji N.}",
year = "1994",
month = "1",
day = "1",
doi = "10.1093/ajcn/59.5.1045",
language = "English (US)",
volume = "59",
pages = "1045--1049",
journal = "American Journal of Clinical Nutrition",
issn = "0002-9165",
publisher = "American Society for Nutrition",
number = "5",

}

Thiamin deficiency impairs endotoxin-induced increases in hepatic glucose output. / Molina, Patricia E.; Yousef, Khalil A.; Smith, Rita M.; Tepper, Patrick G.; Lang, Charles H.; Abumrad, Naji N.

In: American Journal of Clinical Nutrition, Vol. 59, No. 5, 01.01.1994, p. 1045-1049.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Thiamin deficiency impairs endotoxin-induced increases in hepatic glucose output

AU - Molina, Patricia E.

AU - Yousef, Khalil A.

AU - Smith, Rita M.

AU - Tepper, Patrick G.

AU - Lang, Charles H.

AU - Abumrad, Naji N.

PY - 1994/1/1

Y1 - 1994/1/1

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=0028224295&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028224295&partnerID=8YFLogxK

U2 - 10.1093/ajcn/59.5.1045

DO - 10.1093/ajcn/59.5.1045

M3 - Article

VL - 59

SP - 1045

EP - 1049

JO - American Journal of Clinical Nutrition

JF - American Journal of Clinical Nutrition

SN - 0002-9165

IS - 5

ER -