Apoptosis induced by a low-carbohydrate and high-protein diet in rat livers.
OBJECTIVE
To determine whether high-protein, high-fat, and low-carbohydrate diets can cause lesions in rat livers.


METHODS
We randomly divided 20 female Wistar rats into a control diet group and an experimental diet group. Animals in the control group received an AIN-93M diet, and animals in the experimental group received an Atkins-based diet (59.46% protein, 31.77% fat, and 8.77% carbohydrate). After 8 wk, the rats were anesthetized and exsanguinated for transaminases analysis, and their livers were removed for flow cytometry, immunohistochemistry, and light microscopy studies. We expressed the data as mean ± standard deviation (SD) assuming unpaired and parametric data; we analyzed differences using the Student's t-test. Statistical significance was set at P < 0.05.


RESULTS
We found that plasma alanine aminotransferase and aspartate aminotransferase levels were significantly higher in the experimental group than in the control group. According to flow cytometry, the percentages of nonviable cells were 11.67% ± 1.12% for early apoptosis, 12.07% ± 1.11% for late apoptosis, and 7.11% ± 0.44% for non-apoptotic death in the experimental diet group and 3.73% ± 0.50% for early apoptosis, 5.67% ± 0.72% for late apoptosis, and 3.82% ± 0.28% for non-apoptotic death in the control diet group. The mean percentage of early apoptosis was higher in the experimental diet group than in the control diet group. Immunohistochemistry for autophagy was negative in both groups. Sinusoidal dilation around the central vein and small hepatocytes was only observed in the experimental diet group, and fibrosis was not identified by hematoxylin-eosin or Trichrome Masson staining in either group.


CONCLUSIONS
Eight weeks of an experimental diet resulted in cellular and histopathological lesions in rat livers. Apoptosis was our principal finding; elevated plasma transaminases demonstrate hepatic lesions.
Maria Emília L Monteiro, Department of Internal Medicine, Medicine College, Fluminense Federal University, Niterói, RJ 24030-210, Brazil.
Maria Emília L
ME
Monteiro
Maria Emília L Monteiro, Department of Internal Medicine, Medicine College, Fluminense Federal University, Niterói, RJ 24030-210, Brazil.
Analucia R
AR
Xavier
Maria Emília L Monteiro, Department of Internal Medicine, Medicine College, Fluminense Federal University, Niterói, RJ 24030-210, Brazil.
Felipe L
FL
Oliveira
Maria Emília L Monteiro, Department of Internal Medicine, Medicine College, Fluminense Federal University, Niterói, RJ 24030-210, Brazil.
Porphirio Js
PJ
Filho
Maria Emília L Monteiro, Department of Internal Medicine, Medicine College, Fluminense Federal University, Niterói, RJ 24030-210, Brazil.
Vilma B
VB
Azeredo
D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D017209:Apoptosis; D001219:Aspartate Aminotransferases / Q000097:blood; D015415:Biomarkers / Q000097:blood; D050528:Diet, Carbohydrate-Restricted / Q000009:adverse effects*; D004044:Dietary Proteins / Q000633:toxicity*; D005260:Female; D005434:Flow Cytometry; D007150:Immunohistochemistry; D008099:Liver / Q000201:enzymology / Q000473:pathology*; D008107:Liver Diseases / Q000097:blood / Q000209:etiology* / Q000473:pathology; D017208:Rats, Wistar; D013997:Time Factors
D015415:Biomarkers; D004044:Dietary Proteins; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase
Apoptosis; High-fat diet; High-protein diet; Liver injury; Low-carbohydrate diet