Vagus nerve contributes to metabolic syndrome in high-fat diet-fed young and adult rats.
What is the central question of this study? Different nerve contributes periods of life are known for their differential sensitivity to interventions, and increased parasympathetic activity affects the development and maintenance of obesity. Thus, we evaluated the involvement of the vagus nerve by performing a vagotomy in young or adult rats that were offered an obesogenic high-fat diet. What is the main finding and its importance? Although the accumulation of adipose tissue decreased in both younger and older groups, the younger rats showed a greater response to the effects of vagotomy in general. In addition to the important role of the parasympathetic activity, we suggest that the vagus nerve contributes to the condition of obesity. Obesity has become a global problem, and this condition develops primarily because of an imbalance between energy intake and expenditure. The high complexity involved in the regulation of energy metabolism results from several factors besides endocrine factors. It has been suggested that obesity could be caused by an imbalance in the autonomous nervous system, which could lead to a condition of high parasympathetic activity in counterpart to low sympathetic tonus. High-fat (HF) diets have been used to induce obesity in experimental animals, and their use in animals leads to insulin resistance, hyperinsulinaemia and high parasympathetic activity, among other disorders. The aim of this work was to evaluate the effects of a vagotomy performed at the initiation of a HF diet at two different stages of life, weaning and adulthood. The vagotomy reduced parasympathetic activity (-32 and -51% in normal fat-fed rats and -43 and -55% in HF diet-fed rats; P < 0.05) and fat depots (-17 and -33%, only in HF diet-fed rats; P < 0.05). High-fat diet-fed rats exhibited fasting hyperinsulinaemia (fivefold higher in young rats and threefold higher in older rats; P < 0.05); however, vagotomy corrected it in younger rats only, and a similar effect was also observed during the glucose tolerance test. The insulin resistance exhibited by the HF diet-fed groups was not altered in the vagotomized rats. We suggest that the vagus nerve, in addition to the important role of parasympathetic activity, contributes to the condition of obesity, and that non-vagal pathways may be involved along with the imbalanced autonomic nervous system.
Laboratory of Secretion Cell Biology, Department of Biotechnology, Genetics and Cell Biology, State University of Maringá, Maringá, Paraná, Brazil.
Luiz F
LF
Barella
Rosiane A
RA
Miranda
Claudinéia C S
CC
Franco
Vander S
VS
Alves
Ananda
A
Malta
Tatiane A S
TA
Ribeiro
Clarice
C
Gravena
Paulo C F
PC
Mathias
Júlio C
JC
de Oliveira
D050154:Adiposity; D000367:Age Factors; D000818:Animals; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism; D059305:Diet, High-Fat; D004195:Disease Models, Animal; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood / Q000209:etiology* / Q000503:physiopathology / Q000517:prevention & control; D009765:Obesity / Q000097:blood / Q000209:etiology* / Q000503:physiopathology / Q000517:prevention & control; D017208:Rats, Wistar; D013997:Time Factors; D014628:Vagotomy; D014630:Vagus Nerve / Q000503:physiopathology* / Q000601:surgery; D014886:Weaning; D015430:Weight Gain
D015415:Biomarkers; D001786:Blood Glucose; D007328:Insulin