Evidence implicating a specific component of the diet that is most related to increased risk of T2D and obesity remains controversial. Racial/ethnic and sex differences in insulin dynamics exist (29
). In this study, there was a relationship between diet and insulin-related outcomes; however, reported macronutrient intake or quality did not account for racial/ethnic or sex differences in insulin dynamics.
Dietary intake of the children in our sample reflected national trends (33
), exceeding recommendations for simple sugars and saturated fat. In our sample, intake of simple sugar and saturated fat tended to be associated with fasting insulin, as has been reported (33
). In contrast, in our sample, an inverse relationship between CHO and fasting insulin was observed, unlike that which has been noted in samples of older children (34
). Between-study differences in dietary CHO quality, subject maturation status, or the ethnic composition of the subjects may explain different results among studies. In this study, a greater intake of energy from PUFA was associated with greater AIRg. Although PUFA intake is often associated with beneficial health effects, an imbalance in the n-6:n-3 has been associated with hyperinsulinemia and increased insulin secretion (35
). A greater intake of energy from PUFA was associated with greater AIRg in this sample. Our subjects consumed on average an n-6:n-3 of 12:1 (far exceeding the ‘optimal’ 2:1 or 4:1 recommendation), perhaps explaining this observed relationship (data not shown) (35
). Although regional and ethnic variations in the types of foods consumed are apparent in our sample as well as national samples, the macronutrient composition of the diet remains very similar (33
). As such, consumption of “Westernized” diets by most children in the United States may explain why there were no interactions in the dietary and insulin dynamics models (33
The association between diet composition and insulin outcomes may become apparent with age or maturation. Dietary fat (20
) was associated with SI in adolescents, but not younger children. Similar to our results, Lindquist (17
) found no association with any macronutrient and composition and SI in young children. Dietary sugar (22
) was associated with SI among overweight subjects who were on average Tanner stage 2. Puberty is a critical period characterized by insulin resistance and significant changes in body composition and metabolism (29
). Pubertal status could play a role in the interaction between diet and insulin dynamics. To minimize the influence of puberty on insulin-related outcomes, recruitment for our study was limited to individuals between ages 7–12 and ≤pubertal stage 3, which is the time at which the hypothalamic-pituitarygonadal axis matures (36
Puberty is also a sensitive period for fat accumulation and fat accumulation may be influenced by both diet and insulin dynamics. HA in our sample had the greatest adiposity. The contribution of diet to insulin response and action has been observed in older obese HA adolescents (22
) and in AA adolescents, but not EA adolescents (17
). We have previously demonstrated that AA girls (who had greater AIRg), gained more weight over the pubertal transition than their EA counterparts (37
). It has been hypothesized that over time greater insulin secretion may promote greater fat accumulation, which leads to the development of an even greater degree of insulin resistance (38
). We propose that the unique metabolic characteristics that may lead to the pathogenesis of type 2 diabetes are likely to be established during the pubertal transition. Although racial/ethnic differences in insulin dynamics are inherent and are influenced at least in part by a genetic component, it is possible that the obesogenic and insulinogenic diet consumed by the pediatric population adds to this pathogenesis (39
). Although the mechanism by which puberty initiates unique metabolic activity has yet to be elucidated, unhealthy dietary habits, especially during this critical period may have an additive effect over time. Moreover, the additive effect may exhibit a differential impact according to race/ethnicity and sex, and an inter-individual threshold that may differ between racial/ethnic groups. For example, just as other contributors (e.g., intra-abdominal adipose tissue) to adverse metabolic outcomes (e.g., insulin sensitivity) that track over time (40
) may have differential impact among individuals of various racial/ethnic groups, so too may dietary intake. Thus, the multi-factorial perfect storm that occurs over the pubertal transition exacerbates the inherent racial/ethnic differences in insulin dynamics. Although there were few racial/ethnic differences in reported dietary intake, the contribution of diet may have a differential impact on individuals of various racial/ethnic backgrounds with maturation.
In this study, protein intake was associated with lower acute insulin response to glucose. This observation may appear counterintuitive in that protein is a potent insulin secretogogue on an acute basis (43
). However, it is possible that relatively higher chronic protein intake may attenuate the insulin response to glucose. Further, subjects who ate relatively more protein presumable ate relatively less fat and carbohydrate, which may have resulted in an attenuated insulin response to glucose.
Strengths of this study included robust measures of insulin dynamics and body composition. A limitation was its cross-sectional nature preventing the establishment of a cause and effect relationship; longitudinal data will be required to determine if diet influences insulin dynamics over time. In addition, the sample was relatively small and included only healthy, primarily normal-weight (<85th percentile) subjects limiting the generalizablity of the findings. Further, though the sample size was sufficient to detect relationships using the entire sample, when stratified by ethnicity the sample size was limited, thereby possibly restricting the ability to detect ethnic-specific relationships.
In summary, diet likely plays a role in insulin dynamics, though the effect may be additive or interactive with obesity, maturity, and ethnicity. Although diet did not account for racial/ethnic and sex differences in insulin dynamics in our early pubertal children, it is possible that, with maturation and fat deposition, the contribution of diet to insulin dynamics may change in an ethnic-specific manner. These changes may play a role in the increased burden of type 2 diabetes noted among AA and HA relative to EA. Longitudinal studies are needed to determine if diet, via insulin sensitivity or secretion, contributes to disparities in T2D and if the contribution of diet to insulin dynamics strengthens with reproductive maturity.