Exercise training attenuates lipectomy-induced impaired glucose tolerance in rats.
OBJECTIVE
Since visceral adipose tissue (VAT) may account for impaired peripheral and hepatic insulin sensitivity (IS), it has been hypothesized that the partial removal of VAT could result in improved insulin action, while the re-growth of the excised tissue and/or compensatory growth of non-excised depots seems to occur. Thus, it was aimed to investigate whether or not VAT removal and exercise affect IS.


METHODS
Male Wistar rats were fed a high-fat diet and subsequently assigned randomly to one of four groups: 1. exercised plus lipectomized (EL), 2. exercised plus sham-lipectomized (ES), 3. sedentary plus lipectomized (CL), 4. sedentary plus sham-lipectomized (CS). After lipectomy, EL and ES animals underwent a 7-consecutive-day training period. Body weight, food intake, basal metabolic rate, fasting glucose, and glucose tolerance were assessed before and after the interventions. Fasting insulin and the HOMA index, body fat mass, and the expression of pro-inflammatory genes were assessed after the interventions.


RESULTS
EL group showed greater insulin sensitivity compared to all other groups. EL and ES groups showed lower fasting insulin levels when compared to CL and CS groups, respectively. The EL group showed improved IS when compared to the remaining groups. The CL group showed impaired glucose tolerance and increased TNF-alpha gene expression. Body weight and fat mass did not differ among the groups. PPAR gamma gene expression was increased in the EL and ES groups.


CONCLUSIONS
These results showed that short-term swimming training improved insulin sensitivity, but failed to prevent fat regain in lipectomized animals. Lipectomy induced impaired glucose tolerance, which is probably related to increased TNF-alpha gene expression. It is possible that a high-fat diet might be implicated in faster regain of adipose tissue after lipectomy. Our results also show that short-term exercise associated with lipectomy could improve insulin sensitivity.
Coelho
D F
DF
Escola de Educação Física e Esporte, Universidade de São Paulo, SP, Brasil. decoelho@usp.br
Gualano
B
B
Artioli
G G
GG
Roschel
H
H
Amano
M
M
Benatti
F B
FB
Fernandes
T
T
Bueno
C R
CR
Câmara
N O
NO
Lancha
A H
AH
D050153:Abdominal Fat / Q000378:metabolism; D000273:Adipose Tissue / Q000737:chemistry; D050154:Adiposity; D000818:Animals; D001481:Basal Metabolism; D015415:Biomarkers / Q000378:metabolism; D001786:Blood Glucose / Q000032:analysis; D001835:Body Weight; D004032:Diet; D004041:Dietary Fats / Q000008:administration & dosage*; D002149:Energy Intake; D004822:Epididymis; D005215:Fasting / Q000097:blood; D018149:Glucose Intolerance / Q000209:etiology / Q000517:prevention & control*; D005951:Glucose Tolerance Test; D007249:Inflammation / Q000378:metabolism; D007328:Insulin / Q000097:blood; D015187:Lipectomy / Q000009:adverse effects*; D008297:Male; D018482:Muscle, Skeletal / Q000378:metabolism; D047493:PPAR alpha / Q000235:genetics / Q000378:metabolism; D010805:Physical Conditioning, Animal / Q000502:physiology*; D012333:RNA, Messenger / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D013550:Swimming; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism; D015430:Weight Gain / Q000502:physiology*
D015415:Biomarkers; D001786:Blood Glucose; D004041:Dietary Fats; D007328:Insulin; D047493:PPAR alpha; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha