Abstract
Background: Obesity among pregnant women is common, and their offspring are predisposed to obesity, insulin resistance, and diabetes. The circulating metabolites that are related to insulin resistance and are associated with this decreased tissue-specific uptake are unknown. Here, we assessed metabolite profiles in elderly women who were either female offspring from obese mothers (OOM) or offspring of lean mothers (OLM). Metabolic changes were tested for associations with metrics for insulin resistance. Methods: Thirty-seven elderly women were separated into elderly offspring from obese mothers (OOM; n = 17) and elderly offspring from lean/normal weight mothers (OLM; n = 20) groups. We measured plasma metabolites using proton nuclear magnetic resonance (1H-NMR) and insulin-dependent tissue-specific glucose uptake in skeletal muscle was assessed. Associations were made between metabolites and glucose uptake. Results: Compared to the OLM group, we found that the docosahexaenoic acid percentage of the total long-chain n-3 fatty acids (DHA/FA) was significantly lower in OOM (p = 0.015). DHA/FA associated significantly with skeletal muscle glucose uptake (GU) (p = 0.031) and the metabolizable glucose value derived from hyperinsulinemic-euglycemic clamp technique (M-value) in the OLM group only (p = 0.050). Conclusions: DHA/FA is associated with insulin-dependent skeletal muscle glucose uptake and this association is significantly weakened in the offspring of obese mothers.
Highlights
The incidence of obesity and subsequent insulin resistance and type 2 diabetes is rapidly rising
Female offspring of obese mothers have decreased whole-body and muscle glucose uptake compared to elderly female offspring of lean mothers [6], and this suggests that the effects on insulin resistance due to maternal programming may endure over a lifetime
Concentrations were significantly lower in the offspring from obese mothers (OOM) group compared to the OLM group (Table 2, Figure 1B; p = 0.011)
Summary
The incidence of obesity and subsequent insulin resistance and type 2 diabetes is rapidly rising. Maternal obesity predisposes the offspring to insulin resistance starting in utero [5] through fetal programming [6]. As these children become elderly, the consequences of the innate developmental programming leading to insulin resistance and impaired tissue-specific glucose uptake remain unclear. Female offspring of obese mothers have decreased whole-body and muscle glucose uptake compared to elderly female offspring of lean mothers [6], and this suggests that the effects on insulin resistance due to maternal programming may endure over a lifetime. We assessed metabolite profiles in elderly women who were either female offspring from obese mothers (OOM) or offspring of lean mothers (OLM).
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