TY - JOUR
T1 - Food deprivation limits insulin secretory capacity in postpubertal rats
AU - Vuguin, Patricia
AU - Ma, Xiaohui
AU - Yang, Xioman
AU - Surana, Manju
AU - Liu, Bing
AU - Barzilai, Nir
PY - 2001/1
Y1 - 2001/1
N2 - Because prenatal and perinatal undernutrition are associated with type 2 diabetes later in life, we posed the question whether nutrient deprivation during puberty would also result in a decreased ability to secrete insulin. Chronically catheterized, unstressed Sprague Dawley rats, fedad libitum, were studied before puberty (Pre, n= 14) and after puberty (Post, n= 8). Moderately caloric-restricted rats (fed 70% of the control diet, n= 9), were studied after puberty. Insulin secretion was assessed using a hyperglycemic clamp at a glucose concentration of 300 mg/dL, or with a primed continuous infusion of intralipid (plasma FFA levels ˜1.5 mM) at a plasma glucose concentration of 200 mg/dL. Stimulated insulin levels increased in Post rats by 3- to 4-fold compared with Pre rats (from 4.6 ± 0.4 ng/mL Pre to 12.8 ± 0.7 ng/mL Post, and from 4.5 ± 0.4 ng/mL Pre to 15.8 ± 0.7 ng/mL Post, respectively, p“ 0.001, at a glucose concentration of 300 mg/dL, and 200 mg/dL with intralipid). Caloric restriction prevented any rise in insulin secretion (3.8 ± 0.5 and 4.6 ± 0.5 ng/mL in the caloric-restricted rats at glucose concentrations of 300 mg/dL and 200 mg/dL with intralipid, respectively). A semiquantitative reverse-transcriptase PCR procedure was used to assess basal and stimulated insulin mRNA levels. Caloric restriction did not compensate by enhancing insulin mRNA levels in response to glucose stimulation. Moderate food deprivation during puberty reduced the capacity of the pancreas to secrete insulin in response to different nutrient stimuli. We hypothesize that puberty has an important role in -cell maturation and any major nutrient modification may have deleterious consequences later in life.
AB - Because prenatal and perinatal undernutrition are associated with type 2 diabetes later in life, we posed the question whether nutrient deprivation during puberty would also result in a decreased ability to secrete insulin. Chronically catheterized, unstressed Sprague Dawley rats, fedad libitum, were studied before puberty (Pre, n= 14) and after puberty (Post, n= 8). Moderately caloric-restricted rats (fed 70% of the control diet, n= 9), were studied after puberty. Insulin secretion was assessed using a hyperglycemic clamp at a glucose concentration of 300 mg/dL, or with a primed continuous infusion of intralipid (plasma FFA levels ˜1.5 mM) at a plasma glucose concentration of 200 mg/dL. Stimulated insulin levels increased in Post rats by 3- to 4-fold compared with Pre rats (from 4.6 ± 0.4 ng/mL Pre to 12.8 ± 0.7 ng/mL Post, and from 4.5 ± 0.4 ng/mL Pre to 15.8 ± 0.7 ng/mL Post, respectively, p“ 0.001, at a glucose concentration of 300 mg/dL, and 200 mg/dL with intralipid). Caloric restriction prevented any rise in insulin secretion (3.8 ± 0.5 and 4.6 ± 0.5 ng/mL in the caloric-restricted rats at glucose concentrations of 300 mg/dL and 200 mg/dL with intralipid, respectively). A semiquantitative reverse-transcriptase PCR procedure was used to assess basal and stimulated insulin mRNA levels. Caloric restriction did not compensate by enhancing insulin mRNA levels in response to glucose stimulation. Moderate food deprivation during puberty reduced the capacity of the pancreas to secrete insulin in response to different nutrient stimuli. We hypothesize that puberty has an important role in -cell maturation and any major nutrient modification may have deleterious consequences later in life.
UR - http://www.scopus.com/inward/record.url?scp=0035066407&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0035066407&partnerID=8YFLogxK
U2 - 10.1203/00006450-200104000-00006
DO - 10.1203/00006450-200104000-00006
M3 - Article
C2 - 11264428
AN - SCOPUS:0035066407
SN - 0031-3998
VL - 49
SP - 468
EP - 473
JO - Pediatric Research
JF - Pediatric Research
IS - 4
ER -