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Background <p>Maternal fructose intake induces harmful effects in progeny. However, this sugar is not contraindicated during pregnancy. On the other hand, the use of low-calorie sweeteners, such as tagatose, is increasing. Thus, we have studied whether the consumption of tagatose compared to fructose affects lipid metabolism in the offspring of mothers which were supplemented with fructose during their pregnancy.</p> Methods <p>Three-month-old male rat offspring from control or fructose mothers received liquid 10% fructose or tagatose for 21&#xa0;days. A control group (without any additive) was also included. Biochemical and molecular parameters were determined in plasma, tissues and feces.</p> Results <p>Both tagatose and fructose consumption caused hypertriglyceridemia in descendants of fructose-fed mothers. Whereas fructose consumption led to a greater hepatic lipogenesis, tagatose supplementation provoked a higher enterohepatic bile acids recirculation, and therefore a higher intestinal lipid absorption and assembly. However, plasma GLP1, a molecule that affects lipid intestinal absorption, was unchanged. Curiously, FGF21, a molecule which regulates lipid and carbohydrate metabolism and is sensitive to GLP1, was augmented in plasma and liver of tagatose-supplemented descendants regardless of their maternal diet. Interestingly, Angiotensin II (Ang II), which can induce FGF21 production, was increased in plasma of all animals supplemented with tagatose. However, the deleterious effects of Ang II were effectively reversed by FGF21 in males from control mothers, but not in descendants of fructose-fed dams.</p> Conclusions <p>Maternal fructose consumption determines the response of the offspring to tagatose intake, causing an increased intestinal lipid absorption, and metabolic changes that are characteristic of metabolic syndrome such as dyslipidaemia, steatosis and oxidative stress.</p>

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Tagatose consumption provokes metabolic syndrome features in rat males from mothers that consumed fructose during their pregnancy

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月29日

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  • Elena Fauste,
  • Madelín Pérez-Armas,
  • Cristina Donis,
  • Paola Otero,
  • Mª Isabel Panadero,
  • Carlos Bocos

摘要

Background

Maternal fructose intake induces harmful effects in progeny. However, this sugar is not contraindicated during pregnancy. On the other hand, the use of low-calorie sweeteners, such as tagatose, is increasing. Thus, we have studied whether the consumption of tagatose compared to fructose affects lipid metabolism in the offspring of mothers which were supplemented with fructose during their pregnancy.

Methods

Three-month-old male rat offspring from control or fructose mothers received liquid 10% fructose or tagatose for 21 days. A control group (without any additive) was also included. Biochemical and molecular parameters were determined in plasma, tissues and feces.

Results

Both tagatose and fructose consumption caused hypertriglyceridemia in descendants of fructose-fed mothers. Whereas fructose consumption led to a greater hepatic lipogenesis, tagatose supplementation provoked a higher enterohepatic bile acids recirculation, and therefore a higher intestinal lipid absorption and assembly. However, plasma GLP1, a molecule that affects lipid intestinal absorption, was unchanged. Curiously, FGF21, a molecule which regulates lipid and carbohydrate metabolism and is sensitive to GLP1, was augmented in plasma and liver of tagatose-supplemented descendants regardless of their maternal diet. Interestingly, Angiotensin II (Ang II), which can induce FGF21 production, was increased in plasma of all animals supplemented with tagatose. However, the deleterious effects of Ang II were effectively reversed by FGF21 in males from control mothers, but not in descendants of fructose-fed dams.

Conclusions

Maternal fructose consumption determines the response of the offspring to tagatose intake, causing an increased intestinal lipid absorption, and metabolic changes that are characteristic of metabolic syndrome such as dyslipidaemia, steatosis and oxidative stress.