[PHNUTR-L] Propensity for obesity, diabetes, may occur in utero

[Kathrynne Holden, MS, RD]

Colleagues, the following is FYI and does not necessarily reflect my own
opinion. I have no further knowledge of the topic.
------------------------
Public release date: 21-Apr-2005
http://www.eurekalert.org/pub_releases/2005-04/uab-pfo042105.php

Contact: Lois Baker
ljbaker at buffalo.edu
716-645-5000 x1417
University at Buffalo

Propensity for obesity, diabetes, may occur in utero

Studies with rats show permanent “malprogramming” of metabolism, 
appetite center

BUFFALO, N.Y. -- The adage "You are what you eat" should be rephrased to 
include "and so are your children," based on metabolic research 
pioneered by researchers at the University at Buffalo.

Previous studies by the UB scientists showed that rat pups raised 
artificially on a high-carbohydrate milk formula identical in calories 
to mother's milk developed changes in pancreatic islets, resulting in 
overproduction of insulin and obesity in adulthood. The progeny of these 
high-carbohydrate (HC) mothers raised naturally also develop the same 
maladjustments, they found.

The researchers now have shown that this metabolic "malprogramming" is 
permanent and occurs in utero, resulting in the next generation born to 
HC mothers carrying the HC phenotype. Rat fetuses had increased plasma 
insulin levels, increased mRNA levels of preproinsulin, a precursor of 
insulin, and increased insulin in the pancreas, without an increase in 
body weight, plasma glucose level or a change in islet structure.

They also found changes in the hypothalamus, the brain's center of 
appetite regulation, that result in appetite stimulation. While these 
studies were done with rats, Mulchand Patel, Ph.D, UB distinguished 
professor of biochemistry and first author on the study, speculated that 
there is good reason to think the mechanism could be similar in humans.

"Obesity can be perpetuated via the maternal intrauterine environment," 
said Patel, who reported the findings at the 2005 Experimental Biology 
meeting held in San Diego in early April.

"Our earlier studies looked at progeny in the post-weaning period, so we 
didn't know how early this malprogramming occurred. Now we know it 
occurs in utero. We predicted that this could be the case, and our 
present findings support this prediction."

Plasma levels of rat pups (2-HC) born to HC mothers returned to normal 
during the suckling period, results showed, but islets from 12-day-old 
suckling 2-HC rats showed a capacity for insulin oversecretion when 
maintained in culture medium containing high glucose levels. By the 28th 
day, approximately 4 days after weaning to rat chow, 2-HC rats once 
again had high insulin levels and showed a higher capacity for insulin 
secretion to a glucose stimulus. Even on rat chow, body weight began to 
increase around day 55, and 2-HC rats were obese by post-natal day 100.

Patel speculated that in humans, it's possible such malprogramming could 
be interrupted if an obese/insulin resistant mother brought body weight 
and plasma insulin levels back to normal before becoming pregnant.

Malathi Srinivasan. Ph.D, Suhad Shbeir-ElDika, Ravikumar Aalinkeel, 
Ph.D., Fei Song, Ph.D., Lioudmila Pliss, Ph.D., and Paul Mitrani from 
Patel's lab, along with Roberta Pentney, Ph.D., from the UB Department 
of Pathology and Anatomical Sciences, also contributed to the study, as 
well as Shanthie Damodaran, Ph.D., and Sherin Devaskar M.D., from the 
Department of Pediatrics at UCLA, and Brenda Strutt and David Hill 
Ph.D., from the Lawson Research Institute in London, Ontario.
-- 
Kathrynne Holden, MS, RD < fivestar at nutritionucanlivewith.com >
"Ask the Parkinson Dietitian"  http://www.parkinson.org/
"Eat well, stay well with Parkinson's disease"
"Parkinson's disease: Guidelines for Medical Nutrition Therapy"
http://www.nutritionucanlivewith.com/