The realization that low-glycemic index diets were formulated using resistant starch led to more than a decade of research on the health effects of resistant starch. Determination of the metabolizable energy of the resistant starch product allowed for the performance of isocaloric studies. Fermentation of resistant starch in rodent studies results in what appears to be a healthier gut, demonstrated by increased amounts of short-chain fatty acids, an apparent positive change in the microbiota, and increased gene expression for gene products involved in normal healthy proliferation and apoptosis of potential cancer cells. Additionally, consumption of resistant starch was associated with reduced abdominal fat and improved insulin sensitivity. Increased serum glucagon-like peptide 1 (GLP-1) likely plays a role in promoting these health benefits. One rodent study that did not use isocaloric diets demonstrated that the use of resistant starch at 8% of the weight of the diet reduced body fat. This appears to be approximately equivalent to the human fiber requirement. In human subjects, insulin sensitivity is increased with the feeding of resistant starch. However, only 1 of several studies reports an increase in serum GLP-1 associated with resistant starch added to the diet. This means that other mechanisms, such as increased intestinal gluconeogenesis or increased adiponectin, may be involved in the promotion of improved insulin sensitivity. Future research may confirm that there will be improved health if human individuals consume the requirement for dietary fiber and a large amount of the fiber is fermentable.

Physical performance, measured by change in walking speed, was significantly affected by fish oil supplementation. Dietary intake of antioxidants (selenium and vitamin C) and changes in TNFα also contributed to change in walking speed suggesting LCPUFA may interact with antioxidants and inflammatory response to impact physical performance.

Very little is known about the effects of gestational diabetes mellitus (GDM) on lactation and milk components. Recent reports suggested that hyperglycemia during pregnancy was associated with altered breast milk immune factors. Human milk oligosaccharides (HMOs) and N-glycans of milk immune-modulatory proteins are implicated in modulation of infant immunity. The objective of the current study was to evaluate the effect of GDM on HMO and protein-conjugated glycan profiles in breast milk. Milk was collected at 2 wk postpartum from women diagnosed with (n = 8) or without (n = 16) GDM at week 24-28 in pregnancy. Milk was analyzed for HMO abundances, protein concentrations, and N-glycan abundances of lactoferrin and secretory immunoglobulin A (sIgA). HMOs and N-glycans were analyzed by mass spectrometry and milk lactoferrin and sIgA concentrations were analyzed by the Bradford assay. The data were analyzed using multivariate modeling confirmed with univariate statistics to determine differences between milk of women with compared with women without GDM. There were no differences in HMOs between milk from women with vs. without GDM. Milk from women with GDM compared with those without GDM was 63.6% lower in sIgA protein (P < 0.05), 45% higher in lactoferrin total N-glycans (P < 0.0001), 36-72% higher in lactoferrin fucose and sialic acid N-glycans (P < 0.01), and 32-43% lower in sIgA total, mannose, fucose, and sialic acid N-glycans (P < 0.05). GDM did not alter breast milk free oligosaccharide abundances but decreased total protein and glycosylation of sIgA and increased glycosylation of lactoferrin in transitional milk. The results suggest that maternal glucose dysregulation during pregnancy has lasting consequences that may influence the innate immune protective functions of breast milk.

Objective The effects of type 2 resistant starch from high-amylose maize (HAM-RS2) in rodents fed with low-fat diets were demonstrated in previous studies. Fish oil is also reported to reduce body fat. In the current study, the effects of high fat and fish oil on HAM-RS2 feeding in rats were investigated. Design and Methods Rats were fed 0 or 27% (weight) HAM-RS2 with low (15% energy) or high fat (42% energy) diets that included 0 or 10% (energy) tuna oil to test the effect of HAM-RS2 in diet-induced obesity and effects of tuna oil. Data were analyzed as 2 × 2 × 2 factorial. Results Rats fed HAM-RS2 had decreased cecal contents pH, increased cecal and cecal contents weight, increased cecal contents acetate, propionate, and butyrate, increased GLP-1 and PYY, and decreased abdominal fat. However, high fat partially attenuated effects of HAM-RS2, but increased GLP-1 active. Dietary tuna oil had limited effects at concentration used. Conclusions Results demonstrated that a high fat diet partially attenuates the response to HAM-RS2. The mechanism may center on reduced levels of cecal contents propionate and butyrate and reduced serum PYY. This study demonstrated that with consumption of high fat, HAM-RS2 produces fermentation but results in partial attenuation of effects.