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Introduction Vasoactive Intestinal Peptide (VIP) is a 28-amino acid neuropeptide that belongs to the secretin-glucagon superfamily of peptides and has 68% homology with PACAP. VIP is abundantly expressed in the central and peripheral nervous system and in the gastrointestinal tract, where it exercises several physiological functions. Previously, it has been reported that VIP regulates feeding behavior centrally in different species of vertebrates such as goldfishes, chicken, and rodents. Additional studies are necessary to analyze the role of endogenous VIP on the regulation of appetite/satiety together with feeding behavior, metabolic hormone release, body mass composition and energy balance. Aims To elucidate the physiological pathways by which VIP regulates appetite/satiety, feeding behavior, metabolic hormones and body mass composition. Methods VIP deficient (VIP −/−) and age-matched wild-type (WT) littermates were weekly monitored from 5 to 22 weeks of age using a whole body composition EchoMRI analyzer. Food intake and feeding behavior were analyzed using the BioDAQ automated monitoring system. Plasma levels of metabolic hormones including active-ghrelin, GLP-1, leptin, PYY, pancreatic polypeptide (PP), adiponectin, and insulin were measured in fasting as well as in postprandial conditions. Results The genetic lack of VIP led to a significant reduction of body weight and fat mass and to an increase of lean mass as the mice aged. Additionally, VIP−/− mice had a disrupted pattern of circadian feeding behavior resulting in an abolished regular nocturnal/diurnal feeding. These changes were associated with an altered secretion of adiponectin, GLP-1, leptin, PYY and insulin in VIP−/− mice. Our data demonstrates that endogenous VIP is involved in the control of appetite/satiety, feeding behavior, body mass composition and in the secretion of six different key regulatory metabolic hormones. Conclusions Our data show that endogenous VIP is involved in the control of appetite/satiety, feeding behavior, body mass composition and in the secretion of six key regulatory metabolic hormones. VIP plays a key role in the regulation of body weight and mass composition phenotype by significantly enhancing body weight and fat mass accumulation. Therefore, VIP signaling is critical for the modulation of appetite/satiety and body mass phenotype and is suggested to be a target for future treatment of obesity.

The “Latina epidemiologic paradox” refers to the observation that despite socioeconomic disadvantages, Latina mothers in the United States (US) have a similar or lower risk for delivering an infant with low birth weight (LBW) compared to non-Latina White mothers. An analogous paradox may exist between foreign-born (FB) and US-born (USB) Latinas. Our goal was to assess differences in LBW in USB Latinas, FB Latinas, and non-Latina Whites in Los Angeles County in 2003 using birth records and survey data. Using logistic regression, we estimated associations between LBW and birthplace/ethnicity in a birth cohort and nested survey responder group and between LBW and acculturation in responders to a follow-up survey. USB Latinas and FB Latinas had a higher prevalence of LBW infants compared to Whites (odds ratio [OR] = 1.34, 95% confidence interval [CI] = (1.17, 1.53) and OR = 1.32, 95% CI = (1.18, 1.49), respectively); when we adjusted for additional maternal risk factors these point estimates were attenuated, and interval estimates were consistent with a modest positive or inverse association. Among Latinas only, LBW was more common for high-acculturated FB and USB Latinas compared to low-acculturated FB Latinas, and there was limited evidence that environmental or behavior risk factors had less impact in low-acculturated Latinas. In summary, adjusting only for demographics, Latinas in our study were more likely to have LBW infants compared to Whites, in contrast to the Latina paradox hypothesis. Furthermore, adjusting for environmental or behavioral factors attenuated the positive association, but there was little evidence that Latinas had a lower prevalence of LBW regardless of the variables included in the models. Finally, among Latinas, there was limited evidence that associations between known risk factors and LBW were modified by acculturation.

Background Prenatal psychosocial stressors may increase the risk of wheeze in young offspring; yet little attention has been given to the effects that maternal ethnicity may have on this relationship. Methods From a population-based cohort of 1,193 children, we assessed the effect of maternal prenatal stressors on the risk of lifetime wheeze in young offspring. We further studied whether maternal Latina ethnicity modified these associations. Results The risk of wheeze in the offspring was increased from high levels of pregnancy anxiety (aRR 1.40, 95% CI 1.07, 1.83), negative life events (aRR 1.36, 95% CI 1.06, 1.75), or low paternal support (aRR 1.41, 95% CI 1.02, 1.96). The risk of lifetime wheeze was stronger in the offspring of Latina mothers than of White mothers for these same stressors. Discussion Multiple maternal prenatal stressors are associated with increased risk of lifetime wheeze in young offspring, with slight effect modification by Latina ethnicity.