Maternal periodontal disease in rats decreases insulin sensitivity and insulin signaling in adult offspring.
BACKGROUND
Periodontal disease during pregnancy has been recognized as one of the causes of preterm and low-birth-weight (PLBW) babies. Several studies have demonstrated that PLBW babies are prone to developing insulin resistance as adults. Although there is controversy over the association between periodontal disease and PLBW, the phenomenon known as programming can translate any stimulus or aggression experienced during intrauterine growth into physiologic and metabolic alterations in adulthood. The purpose of the present study is to investigate whether the offspring of rats with periodontal disease develop insulin resistance in adulthood.


METHODS
Ten female Wistar rats were divided into periodontal disease (PED) and control (CN) groups. All rats were mated at 7 days after induction of periodontal disease. Male offspring were divided into two groups: 1) periodontal disease offspring (PEDO; n = 24); and 2) control offspring (CNO; n = 24). Offspring body weight was measured from birth until 75 days. When the offspring reached 75 days old, the following parameters were measured: 1) plasma concentrations of glucose, insulin, fructosamine, lipase, amylase, and tumor necrosis factor-α (TNF-α); 2) insulin sensitivity (IS); and 3) insulin signal transduction (IST) in insulin-sensitive tissues.


RESULTS
Low birth weight was not detected in the PEDO group. However, plasma concentrations of glucose, insulin, fructosamine, lipase, amylase, and TNF-α were increased and IS and IST were reduced (P <0.05) in the PEDO group compared with the CNO group.


CONCLUSIONS
Maternal periodontal disease may induce insulin resistance and reduce IST in adult offspring, but such alterations are not attributable to low birth weight.
Department of Basic Sciences, Dental School of Araçatuba, São Paulo State University, São Paulo, São Paulo, Brazil.
Daisy J
DJ
Shirakashi
Rosana P
RP
Leal
Natalia H
NH
Colombo
Fernando Y
FY
Chiba
Cléa A S
CA
Garbin
Elerson G
EG
Jardim
Cristina
C
Antoniali
Doris H
DH
Sumida
D000681:Amylases / Q000097:blood; D000818:Animals; D000831:Animals, Newborn; D001724:Birth Weight; D001786:Blood Glucose / Q000032:analysis; D005260:Female; D019270:Fructosamine / Q000097:blood; D007328:Insulin / Q000097:blood / Q000378:metabolism*; D007333:Insulin Resistance / Q000502:physiology*; D008049:Lipase / Q000097:blood; D008297:Male; D010518:Periodontitis / Q000097:blood / Q000000981:diagnostic imaging / Q000503:physiopathology*; D011247:Pregnancy; D011248:Pregnancy Complications / Q000503:physiopathology*; D011297:Prenatal Exposure Delayed Effects; D011859:Radiography; D051381:Rats; D017208:Rats, Wistar; D015398:Signal Transduction; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
D001786:Blood Glucose; D007328:Insulin; D014409:Tumor Necrosis Factor-alpha; D019270:Fructosamine; D008049:Lipase; D000681:Amylases