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High Fructose Diet in Mice Activates Brainstem Angiotensin AT1a and Catecholaminergic Systems
Author(s) -
Farah Vera,
Elased Khalid M.,
Chen Yanfang,
Key Mary,
Cunha Tatiana S.,
Aguiar Janaina P.,
Pazzine Mariana,
Irigoyen Maria Claudia,
Morris Mariana
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a300
Subject(s) - medicine , endocrinology , fructose , in situ hybridization , angiotensin ii , chemistry , catecholaminergic , biology , receptor , messenger rna , catecholamine , biochemistry , gene
A high fructose diet produces glucose resistance in animals and humans. Previous studies from our laboratory showed that fructose feeding in mice produced an increase in plasma angiotensin (Ang) II associated with a mild hypertension and sympathetic activation which was observed only during the dark phase. The aim of this study was to evaluate the effect of consumption of a high fructose diet on brainstem Ang and catecholaminergic systems. Using in situ hybridization methods we identified and quantified Ang AT1a and tyrosine hydroxylase (TH) mRNA in brainstem regions involved in cardiovascular regulation, locus coeruleus (LC) and dorsal vagal complex (DVC). Male C57BL mice were fed a normal chow (Control, n=6) or a fructose‐rich diet (60%, n=7) for 8 weeks. Dietary fructose produced no change in body weight, glucose or insulin. Fructose produced impairment in glucose tolerance and increased plasma cholesterol. There was a significant increase in expression of Ang AT1a and TH mRNA in the LC of fructose‐fed mice (60–70% increase) as measured using phosphor imaging methods. Fructose did not change mRNA expression in the DVC. Emulsion photomicrographs showed that there is a clear co‐distribution of Ang AT1a and TH mRNA in the LC and DVC. Results show that a high fructose diet activates Ang AT1a receptor and TH mRNA in a cardiovascular responsive brainstem region. These central changes may mediate the dietary induced cardiovascular effects