[PHNUTR-L] Propensity for obesity, diabetes, may occur in utero
Kathrynne Holden, MS, RD
fivestar at nutritionucanlivewith.com
Mon Apr 25 15:28:42 PDT 2005
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
Contact: Lois Baker
ljbaker at buffalo.edu
University at Buffalo
Propensity for obesity, diabetes, may occur in utero
Studies with rats show permanent “malprogramming” of metabolism,
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"
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