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1.
Prev Med ; 153: 106723, 2021 12.
Artículo en Inglés | MEDLINE | ID: mdl-34271075

RESUMEN

Impaired mobility is the most common form of functional disability in the US, affecting one out of every sixteen working-age adults. Little is known about the barriers to and facilitators of healthy eating among people with impaired mobility (PWIM), who are at increased risk for diet-related chronic disease. The pathways by which impaired mobility influence dietary intake are unclear, yet likely involve a complex interplay between structural determinants of health and individual factors. To help advance nutrition equity initiatives for PWIM, this systematic review aimed to qualitatively synthesize factors associated with dietary intake across four levels of ecologic influence. An interprofessional team devised a comprehensive search strategy to identify these factors among working-age (18-64 years) PWIM. We queried Ovid MEDLINE, Web of Science, Scopus, and Embase via Ovid for articles published between January 1, 1990 and April 25, 2021. Twelve studies met our review criteria. We classified factors within one of four ecologic levels of influence: individual, social, environmental, and policy/program. Most studies disproportionately reported on personal level factors of influence, with less information on other levels of influence. This systematic review is an important first step for informing the design of evidence-based strategies to support healthy eating among PWIM. However, it also reveals a wide chasm in the needed information to adequately bridge structural determinants of this nutrition divide. More studies are needed that include rigorous measures of dietary intake and that aim to elicit how social, environmental, and policy-level factors contribute to dietary disparities among PWIM.


Asunto(s)
Dieta Saludable , Dieta , Adolescente , Adulto , Ingestión de Alimentos , Humanos , Persona de Mediana Edad , Estado Nutricional , Adulto Joven
2.
Hepatology ; 70(1): 276-293, 2019 07.
Artículo en Inglés | MEDLINE | ID: mdl-30983011

RESUMEN

Pregnancy is associated with progressive hypercholanemia, hypercholesterolemia, and hypertriglyceridemia, which can result in metabolic disease in susceptible women. Gut signals modify hepatic homeostatic pathways, linking intestinal content to metabolic activity. We sought to identify whether enteric endocrine signals contribute to raised serum bile acids observed in human and murine pregnancies, by measuring fibroblast growth factor (FGF) 19/15 protein and mRNA levels, and 7α-hydroxy-4-cholesten-3-one. Terminal ileal farnesoid X receptor (FXR)-mediated gene expression and apical sodium bile acid transporter (ASBT) protein concentration were measured by qPCR and western blotting. Shotgun whole-genome sequencing and ultra-performance liquid chromatography tandem mass spectrometry were used to determine the cecal microbiome and metabonome. Targeted and untargeted pathway analyses were performed to predict the systemic effects of the altered metagenome and metabolite profiles. Dietary CA supplementation was used to determine whether the observed alterations could be overcome by intestinal bile acids functioning as FXR agonists. Human and murine pregnancy were associated with reduced intestinal FXR signaling, with lower FGF19/15 and resultant increased hepatic bile acid synthesis. Terminal ileal ASBT protein was reduced in murine pregnancy. Cecal bile acid conjugation was reduced in pregnancy because of elevated bile salt hydrolase-producing Bacteroidetes. CA supplementation induced intestinal FXR signaling, which was not abrogated by pregnancy, with strikingly similar changes to the microbiota and metabonome as identified in pregnancy. Conclusion: The altered intestinal microbiota of pregnancy enhance bile acid deconjugation, reducing ileal bile acid uptake and lowering FXR induction in enterocytes. This exacerbates the effects mediated by reduced bile acid uptake transporters in pregnancy. Thus, in pregnant women and mice, there is reduced FGF19/15-mediated hepatic repression of hepatic bile acid synthesis, resulting in hypercholanemia.


Asunto(s)
Ácidos Cólicos/sangre , Microbioma Gastrointestinal , Reabsorción Intestinal , Embarazo/sangre , Receptores Citoplasmáticos y Nucleares/metabolismo , Amidohidrolasas/genética , Animales , Bacteroides/aislamiento & purificación , Ciego/efectos de los fármacos , Ciego/microbiología , Ácidos Cólicos/farmacología , Enterocitos/efectos de los fármacos , Femenino , Humanos , Ratones Endogámicos C57BL , Receptores Citoplasmáticos y Nucleares/agonistas
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