Environmental and biologic interactions on behavior: Effects of artificial rearing in rat pups treated with 6-hydroxydopamine

1982 ◽  
Vol 15 (4) ◽  
pp. 297-307 ◽  
Author(s):  
James R. Goldenring ◽  
Bennett A. Shaywitz ◽  
Robert S. Wool ◽  
David K. Batter ◽  
George M. Anderson ◽  
...  
1990 ◽  
Vol 23 (2) ◽  
pp. 169-178 ◽  
Author(s):  
Elizabeth Moore ◽  
Colleen Stamper ◽  
Jaime Diaz ◽  
Elise Murowchick
Keyword(s):  

2009 ◽  
Vol 66 (3) ◽  
pp. 272-277 ◽  
Author(s):  
Cynthia B de Medeiros ◽  
Alison S Fleming ◽  
Celeste C Johnston ◽  
Claire-Dominique Walker

2003 ◽  
Vol 228 (1) ◽  
pp. 15-23 ◽  
Author(s):  
Malathi Srinivasan ◽  
Suzanne G. Laychock ◽  
David J. Hill ◽  
Mulchand S. Patel

Obese individuals are more likely to suffer from diseases termed the “metabolic syndrome,” which includes type 2 diabetes. It is now recognized that early life dietary experiences play an important role in the etiology of such diseases. In this context, the consequences of a high carbohydrate (HC) dietary intervention in neonatal rats is being studied in our laboratory. Artificial rearing of 4-day-old rat pups on a HC milk formula up to Day 24 results in the immediate onset of hyperinsulinemia, which persists throughout the period of dietary intervention. Several adaptations at the biochemical, cellular, and molecular levels in the islets of these HC rats support the onset and persistence of the hyperinsulinemic condition during this period. Some of these adaptations include a distinct leftward shift in the insulin secretory capacity, increased hexokinase activity, increased gene expression of preproinsulin and related transcription factors and specific kinases in 12-day-old HC islets, and alterations in the number and size of islets. These adaptations are programmed and expressed in adulthood thereby sustain the hyperinsulinemic condition in the postweaning period and form the basis for adult-onset obesity. HC females spontaneously transmit the HC phenotype (chronic hyperinsulinemia and adult-onset obesity) to their progeny. Collectively, our results indicate that even a mere switch in the nature of the source of calories (from fat rich in rat milk to carbohydrate rich in the HC milk formula) during critical phases of early development in the rat results in metabolic programming of islet functions leading to chronic hyperinsulinemia (throughout life) and adult-onset obesity. This metabolic programming, once established, forms a vicious cycle because HC female rats spontaneously transmit the HC phenotype to their progeny. The results from our laboratory in the context of metabolic programming due to neonatal nutritional experiences are discussed in this review.


1983 ◽  
Vol 49 (3) ◽  
pp. 497-506 ◽  
Author(s):  
J. L. Smart ◽  
D. N. Stephens ◽  
H. B. Katz

1. In order to exclude the possibility of differences in maternal care which are known to result from typical methods of undernutrition during the suckling period, rat pups were reared artificially on different planes of nutrition away from their mothers.2. Artificial rearing was accomplished by fitting infant rats with a gastric cannula through which a milk substitute was infused intermittently. Rats were fed thus from 4 to 21 d on a high (ARHI) or a low (ARLO; 44% of ARHI level) plane of nutrition. Underfeeding of the ARLO group was continued till 25 d, after which all rats were given a good-quality pelleted diet ad lib.3. Compared with mother-reared (MR) litter-mates, ARHI rats showed advanced eye-opening and, at 21 and 25 d, they resisted restraint more strongly.4. Growth in body-weight of ARHI and MR rats was similar but, when autopsied at 32 weeks, the ARHI rats were shorter (nose–rump length) and had lighter gastrocnemius muscles, adrenals and brains, but heavier epididymal-fat pads.5. ARLO rats had deficits at 32 weeks compared with ARHI rats in whole body, kidney and epididymal-fat-pad weights, and in tibia length.6. In a second experiment, ARHI and MR rats were killed at 21 d. All the differences found at 32 weeks were already present at 21 d. In addition, the ARHI pups had enlarged livers and intestines but shorter tibias.7. The milk substitute, which is one commonly used in such studies, has a low protein and high carbohydrate content compared with rats' milk. This difference probably caused the abnormal organ growth of ARHI rats.


1994 ◽  
Vol 14 (1) ◽  
pp. 21-40 ◽  
Author(s):  
Mulchand S. Patel ◽  
Satyaprasad Vadlamudi ◽  
Gary L. Johanning

1982 ◽  
Vol 112 (5) ◽  
pp. 841-847 ◽  
Author(s):  
Jaime Diaz ◽  
Elizabeth Moore ◽  
Frances Petracca ◽  
Jack Schacher ◽  
Colleen Stamper
Keyword(s):  

1979 ◽  
Vol 22 (1) ◽  
pp. 69-75 ◽  
Author(s):  
Mark Piccirillo ◽  
Donald J. Cohen ◽  
Bennett A. Shaywitz ◽  
Jonathan E. Alpert ◽  
David Marinelli

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