Maternal Nutrition and Fetal Origins of Adult Metabolic Diseases

Assessing the impact of maternal nutrition on health of the offspring in humans is difficult. However, investigations involving offspring conceived during conditions of famine have provided direct evidence of the effects that maternal nutrition during gestation and lactation has on the overall health of the adult offspring. The Dutch famine, which occurred in the western part of the Netherlands at the end of World War II, only lasted around 5 months from late November 1944 to early May 1945, and was therefore defined as a short period of famine. Prior to the onset of the famine conditions, the affected area of the Netherlands consisted of a reasonably well-nourished population. The occurrence of this abrupt famine therefore granted researchers a unique opportunity to retrospectively study the effect of maternal nutrition during specific stages of gestation on insulin-glucose homeostasis and obesity risk in adult offspring (Table 2).

Investigators traced and studied individuals who were born immediately before the famine commenced, those born during the famine, and those born up to 21 months after the famine had ceased. Compared to the offspring not exposed to in utero famine conditions, individuals who were in utero during the famine had higher plasma glucose levels

Table 2 Effects of famine conditions during the different stages of pregnancy

Maternal exposure to famine Maternal exposure to famine during pre-early gestation during mid-late gestation

Table 2 Effects of famine conditions during the different stages of pregnancy

Maternal exposure to famine Maternal exposure to famine during pre-early gestation during mid-late gestation

Increased birth weight

Reduced birth weight

Increased birth length

Reduced birth length

Increased obesity

Reduced glucose tolerance

Increased risk of coronary

Increased risk of type 2

heart disease

diabetes

2 h after a standard oral glucose tolerance test. These glucose levels were highest in those individuals who had been exposed to the famine during the final trimester of pregnancy and then become obese in adult life. In terms of obesity, individuals who were exposed to the famine during the first half of pregnancy were more obese at age 19 years. In contrast those who were exposed to the famine during the last trimester of pregnancy and in early postnatal life had reduced obesity. This suggests that the critical time windows for increased risk of obesity and type 2 diabetes differ. This study provided direct evidence that poor maternal nutrition leads to increased susceptibility of type 2 diabetes and obesity in offspring. It also supports the hypothesis that the greatest risk of developing metabolic diseases exists when there is a marked conflict between the environmental conditions experienced in utero and that experienced in adult life.

As nutritional studies in humans are complex and clouded by multiple confounding factors, a number of animal models of maternal nutritional insults have been developed. Investigations involving these models have significantly contributed to elucidating pathogenic mechanisms underlying the fetal origins of adult metabolic diseases.

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