Obese ZDF rats fermented resistant starch with effects on gut microbiota but no reduction in abdominal fat.

SCOPE: To determine if whole-grain (WG) flour with resistant starch (RS) will produce greater fermentation than isolated RS in obese Zucker Diabetic Fatty (ZDF) rats, and whether greater fermentation results in different microbiota, reduced abdominal fat, and increased insulin sensitivity. METHODS AND RESULTS: This study utilized four groups fed diets made with either isolated digestible control starch, WG control flour (6.9% RS), isolated RS-rich corn starch (25% RS), or WG corn flour (25% RS). ZDF rats fermented RS and RS-rich WG flour to greatest extent among groups. High-RS groups had increased serum glucagon-like peptide 1 (GLP-1) active. Feeding isolated RS showed greater Bacteroidetes to Firmicutes phyla among groups, and rats consuming low RS diets possessed more bacteria in Lactobacillus genus. However, no differences in abdominal fat were observed, but rats with isolated RS had greatest insulin sensitivity among groups. CONCLUSIONS: Data demonstrated ZDF rats (i) possess a microbiota that fermented RS, and (ii) WG high-RS fermented better than purified RS. However, fermentation and microbiota changes did not translate into reduced abdominal fat. The defective leptin receptor may limit ZDF rats from responding to increased GLP-1 and different microbiota for reducing abdominal fat, but did not prevent improved insulin sensitivity.

Simultaneous delivery of antibiotics neomycin and ampicillin in drinking water inhibits fermentation of resistant starch in rats.

SCOPE: Antibiotics ampicillin 1 g/L and neomycin 0.5 g/L were added to drinking water before or during feeding of resistant starch (RS) to rats to inhibit fermentation. METHODS AND RESULTS: In a preliminary study, antibiotics and no RS were given prior to rats receiving a transplant of cecal contents via gavage from donor rats fed RS (without antibiotics) or a water gavage before feeding resistant starch to both groups. Antibiotics given prior to feeding RS did not prevent later fermentation of RS regardless of either type of gavage. In the second study, antibiotics were given simultaneously with feeding of RS. This resulted in inhibition of fermentation of RS with cecal contents pH >8 and low amounts of acetate and butyrate. Rats treated with antibiotics had reduced Bifidobacteria spp., but similar Bacteroides spp. to control groups to reduce acetate and butyrate and preserve the production of propionate. Despite reduced fermentation, rats given antibiotics had increased glucagon-like peptide 1 (GLP-1) and cecum size, measures that are usually associated with fermentation. CONCLUSIONS: A simultaneous delivery of antibiotics inhibited fermentation of RS. However, increased GLP-1 and cecum size would be confounding effects in assessing the mechanism for beneficial effects of dietary RS by knocking out fermentation.

Role of resistant starch in improving gut health, adiposity, and insulin resistance.

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.

Resistant starch from high amylose maize (HAM-RS2) and dietary butyrate reduce abdominal fat by a different apparent mechanism.

OBJECTIVE: Obesity is a health concern. Resistant starch (RS) type 2 from high-amylose maize (HAM-RS2) and dietary sodium butyrate (SB) reduce abdominal fat in rodents. RS treatment is associated with increased gut hormones peptide YY (PYY) and glucagon-like peptide 1 (GLP-1), but it is not known if SB increases these hormones. DESIGN AND METHODS: This was investigated in a 2 × 2 rat study with HAM-RS2 (0 or 28% weight) and dietary sodium butyrate (0 and 3.2%) resulting in isocaloric treatments: energy control (EC), sodium butyrate (SB), HAM-RS2 (RS), and the combination (SBRS). RESULTS: RS and SB reduced abdominal fat and the combination reduced abdominal fat compared to SB and RS. RS was associated with increased fermentation in the cecum. Serum PYY and GLP-1 total were increased with RS treatment. RS treatment was associated with increased cecal butyrate produced from fermentation of RS, but there was no cecal increase for dietary SB. CONCLUSIONS: SB after its absorption into the blood appears to not affect production of PYY and GLP-1, while butyrate from fermentation in the cecum promotes increased PYY and GLP-1. Future studies with lower doses of RS and SB are warranted and the combination may be beneficial for human health.

Navigating the current job market--grab hold of your future now!

Although the U.S. federal government, the National Science Foundation, and other influential groups have called for American universities to educate and train more scientists, a recent article in the Washington Post and broadcasting on National Public Radio affirmed a harsh reality: there are too few jobs for today's young scientists. Essentially, landing a job in science doesn't just happen, you must prepare! The intent of this education track session, targeted to students, postdoctorates, junior faculty, and other early- to midcareer professionals was to provide insights on trends in the current job market and offer strategies and resources to be competitive. The session featured speakers representing different work environments, such as academia, industry, health care institutions, public relations, and entrepreneurial positions.

Human milk secretory immunoglobulin a and lactoferrin N-glycans are altered in women with gestational diabetes mellitus.

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.

Resistant starch from high amylose maize (HAM-RS2) reduces body fat and increases gut bacteria in ovariectomized (OVX) rats.

OBJECTIVE: Obesity after menopause is a health concern for older females. Changes in the microbiota are likely to occur with this condition. Modifying the microbiota with a prebiotic is a plausible strategy for improving the health of menopausal females. DESIGN AND METHODS: Resistant starch type 2 from high-amylose maize (HAM-RS2) was used as a prebiotic in rats in a 2 × 2 factorial study with two levels of HAM-RS2 (0 or 29.7% of weight of diet) referred to as energy control (EC) and HAM-RS2 diets, respectively; and two levels of surgery, ovariectomized (OVX) and sham. RESULTS: In a 6-week, postsurgery recovery period, OVX rats gained more body weight with consumption of a similar amount of food. Subsequently, consumption of HAM-RS2 versus EC diets resulted in reduced abdominal fat in both OVX and sham rats; but when normalized for disemboweled body weight (body weight minus GI tract), there was no effect of surgery, only reduction with HAM-RS2. Targeted bacterial populations were estimated that are known to ferment HAM-RS2 or metabolize the products of that initial fermentation. OVX and sham rats demonstrated increased bacterial levels with dietary HAM-RS2 for all bacteria. Additionally, culture techniques and qPCR provided similar results. CONCLUSION: This study shows that, as expected, OVX increases adiposity. However, contrary to previous effects seen in obese mice, this did not prevent fermentation of HAM-RS2 and consequently, the fat gain associated with OVX was attenuated.

High fat diet partially attenuates fermentation responses in rats fed resistant starch from high-amylose maize.

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.

Postpartum physical activity in overweight and obese women.

BACKGROUND: Low physical activity (PA) during the postpartum period is associated with weight retention. While patterns of PA have been examined in normal weight women during this period, little is known about PA among overweight and obese women. The aim of this cross-sectional study was to investigate PA and determine the proportion of women meeting recommendations for PA. METHODS: Women (n = 491), with a body mass index (BMI) ≥ 25 kg/m² were enrolled in a behavioral intervention. PA was assessed at six weeks postpartum using the Seven-Day PA Recall. RESULTS: Women averaged 923 ± 100 minutes/day of sedentary/ light and 33 ± 56 minutes/day of combined moderate, hard, and very hard daily activity. Women with a BMI ≥ 40 kg/m² reported more time in sedentary/light activities and less hours of sleep than those with a lower BMI. Only 34% met national PA guidelines; this proportion was significantly lower among blacks (OR 0.5, CI 0.3-0.9). CONCLUSIONS: These overweight and obese postpartum women reported a large percentage of time spent in sedentary/light activity, and a high proportion failed to meet minimal guidelines for PA. Promotion of PA in the postpartum period should focus on reducing sedentary behaviors and increasing moderate PA.

Comparison of dietary intake of overweight postpartum mothers practicing breastfeeding or formula feeding.

BACKGROUND: Weight gain in the postpartum period is a risk factor for long-term obesity. Investigations of dietary intake among lactating and nonlactating overweight women might identify nutritional concerns specific to this population. OBJECTIVE: To compare nutrient, meal, and snack intakes, food-group servings and prevalence of dieting among fully breastfeeding (BF), mixed breast and formula feeding (MF), and formula feeding (FF) overweight and obese women. The second aim was to compare nutrient intakes and food-group servings to the Dietary Reference Intake and MyPyramid recommendations, respectively. DESIGN: Data were collected from September 2004 through April 2006 in Durham, NC. Infant feeding practices and dietary information were collected on 450 women between 6 and 9 weeks postpartum. Two 24-hour dietary recalls were completed by phone, using Nutrition Data Systems for Research. Analysis of covariance was used to compare infant feeding groups in dietary quality (nutrient intake per 1,000 kcal) and food-group servings, controlling for prepregnancy body mass index, race, age, education, income, and marital status. χ² analysis was performed to determine differences in meal and snack intake and dieting among infant feeding groups. RESULTS: BF women consumed more energy (2,107 ± 50 kcal) than MF (1,866 ± 56 kcal) or FF (1,657 ± 50 kcal) women (P < 0.001). Adjusted nutrient intake did not differ between groups. All groups were at risk for inadequate intakes of vitamins A, E, C, and folate and did not meet recommended servings of all food groups. BF women consumed lunch and snacks more frequently, were less likely to diet, and reported higher intakes of grains and desserts than MF and FF women. CONCLUSIONS: To help increase intakes of nutrients lacking in the diet and prevent postpartum weight gain, overweight women should be encouraged to increase fruits, vegetables, low-fat dairy, whole grains, legumes, and healthy types of fat, while decreasing refined grains, regular soda, sweetened beverages, and desserts.

Development of insulin resistance and hyperphagia in Zucker fatty rats.

The onset of hyperphagia in the Zucker fatty (fa/fa) rat occurs on a single day in postnatal development and could be driven by an increase in insulin sensitivity. To test this hypothesis, we performed insulin tolerance tests at several points in development. In rapidly growing juvenile rats, fatty rats are as insulin sensitive as lean rats at 4 wk of age but become increasingly insulin resistant as they became obese. During the suckling to weaning transition, fatty rats are insulin resistant at 2 wk of age, when they are exclusively suckling; they are also insulin resistant at 3 wk of age, when they are suckling and consuming solid food, but not hyperphagic. By 4 wk of age, when fatty rats are hyperphagic, they are as insulin sensitive as their lean littermates. These data indicate that fatty rats experience two phases of insulin resistance, punctuated by a brief period of insulin sensitivity that follows the onset of hyperphagia. To determine whether the increase in insulin sensitivity could be driving the onset of hyperphagia, insulin tolerance tests were performed from 21 to 27 days of age. Obese and lean rats became increasingly insulin resistant from 21 to 23 days of age and then became as insulin sensitive as lean rats by 25 days of age. These data show that increased insulin resistance precedes the onset of hyperphagia and increased insulin sensitivity follows the onset of hyperphagia. This pattern suggests that developmental perturbations in insulin signaling are likely to be involved in the onset of hyperphagia.