Invert sugar induces glucose intolerance but does not cause injury to the pancreas nor permanent DNA damage in rats.

An Acad Bras Cienc

Programa de Pós-Graduação em Promoção da Saúde, Universidade de Santa Cruz do Sul/UNISC, Santa Cruz do Sul, RS, Brazil.

Published: September 2020

AI Article Synopsis

  • Eating too much sugar can lead to obesity and prediabetes, but not much is known about how a specific sugar called invert sugar affects our bodies.
  • In a study with rats, researchers found that those who ate a lot of invert sugar got fatter and had trouble processing sugar, but their pancreas and liver weren't seriously harmed.
  • The study showed that while high invert sugar intake caused some temporary DNA damage in the blood, it didn't seem to cause long-term damage to the rats' organs.

Article Abstract

The high consumption of sugars is linked to the intermediate hyperglycemia and impaired glucose tolerance associated with obesity, inducing the prediabetes. However, the consequences of excessive invert sugar intake on glucose metabolism and genomic stability were poorly studied. The aim of this study was to evaluate the effects of invert sugar overload (32%) in rats, analyzing changes in obesity, glucose tolerance, pancreatic/hepatic histology and primary and permanent DNA damage. After 17 weeks, the rats became obese and had an excessive abdominal fat, as well as presented impaired glucose tolerance, caused by higher sugar caloric intake. Primary DNA damage, evaluated by the comet assay, was increased in the blood, however not in the pancreas. No protein carbonylation was seen in serum. Moreover, no increase in permanent DNA damage was seen in the bone marrow, evaluated using the micronucleus test. Some rats presented liver steatosis and that the pancreatic islets were enlarged, but not significantly. In this study, invert sugar altered the glucose metabolism and induced primary DNA damage in blood, but did not cause significant damage to the pancreas or liver, and neither changes in the levels of oxidative stress or permanent DNA damage.

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Source
http://dx.doi.org/10.1590/0001-3765202020191423DOI Listing

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