Recovery of rat growth and lipid profiles in adult rats subjected to fetal protein malnutrition with a fructose-rich diet

Abstract

There is evidence suggesting an association between fructose consumption and the development of metabolic syndrome. In turn, protein malnutrition in utero is proposed to "program" the fetal tissues, making them more susceptible to nutritional associated disorders. To test this hypothesis, the present study was designed to analyze body growth and metabolic aspects of rats subjected to fetal protein malnutrition and subsequently fed a fructose-rich diet. Wistar rats were distributed into 4 groups: balanced (B) diet-B diet offered the entire experimental period; balanced diet/fructose-B diet until birth and fructose-rich diet (F-60% fructose) until adulthood; low-protein (L) diet/balanced-L diet until birth and B diet until adulthood; low-protein diet/fructose (F)-L diet until birth and F diet until adulthood. After nutritional recovery, there was a restoration of serum glucose, total protein, and albumin concentrations, which were reduced by fetal malnutrition, and a restoration of the liver glycogen and lipids contents, which were increased by fetal malnutrition. This restoration was independent of the diet adopted after birth. It was verified that the high fructose diet arrested body growth of the rats independently of the nutritional state during fetal life and was associated with weight reduction and decrease of the adipose in some regions of the body (P < .05). Moreover, the serum concentrations of triglycerides and total cholesterol, which are indicators of metabolic syndrome, rose in the rats that ingested the fructose-rich diet (P < .05). In summary, high consumption of fructose impairs body growth and alters the circulating lipids independently of the protein nutrition in utero.

Plasma lipid levels and body weight altered by intrauterine growth restriction and postnatal fructose diet in adult rats

“…This could be due to the production of large, triglyceride-rich very-low-density lipoprotein particles not converted to LDL but cleared from plasma by the remnant receptors. One study elucidated the interaction between maternal protein restriction and immediate postnatal fructose, and it was concluded that the offspring were not more susceptible to the effects of fructose diet (33).…”

Fructose, pregnancy and later life impacts

“…143 However, "maternal fructose intake alters offspring development" fetal protein malnutrition and subsequent postnatal elevated fructose intake appear to arrest the body growth, specifically in the adipose tissue mass, of rats independent of the nutritional state during fetal life. 97 Interestingly, these changes were not associated with impaired glucose tolerance or the development of whole-body insulin resistance. 97 These types of studies provide an important basis on which future studies can be conducted.…”

“…97 Interestingly, these changes were not associated with impaired glucose tolerance or the development of whole-body insulin resistance. 97 These types of studies provide an important basis on which future studies can be conducted. They are beginning to shed light on the interaction between the in utero environment (different insults and their timing) and postnatal dietary environment.…”

“…The paucity of these studies and the lack of human studies, given the increased maternal consumption of fructose-sweetened foods and the links between adverse in utero environments and later life associations with metabolic disorders, 15,17,97,110,111 highlight the need for continuing investigations to further clarify the impact of elevated fructose consumption on the early life period and implications for adult disease risk.…”

“…This biochemical difference in structure and fructose concentration may result in different metabolic outcomes. Comparing the effects of sucrose or glucose and HFCS ingestion on acute metabolic and haemodynamic parameters demonstrates that the ingestion of 90,100,108,110,[112][113][114]133 10% v/v tap water GDM, altered placental vessel development, sex-specific weight effects and hypertriglyceridaemia 63% feed GDM and increased liver TAG Fetus 20% and 10% v/v in water Reductions in placental/birth weights 100,117 10%, 50% and 60% v/v in water Fetal hyperglycaemia and hypertriglyceridaemia and changes in fetal liver weight and genes 90,95,114,[131][132][133] Lactation~60% v/v drinking water Altered calcium metabolism 136 Offspring 10% and 20% v/v drinking water Sex effects, bodyweight, fat depot and hypothalamic changes 97,99,100,140 In utero environment modulation of growth prior to postnatal fructose exposure OR, odds ratio; GDM, gestational diabetes mellitus; TAG, triacylglycerol.…”