Do Neighborhoods Matter? A Systematic Review of Modifiable Risk Factors for Obesity among Low Socio-Economic Status Black and Hispanic Children.

BACKGROUND: Childhood obesity increases the risk of obesity and harmful comorbidities later in life. It is influenced by characteristics of a child's neighborhood, particularly among underserved groups. Our objective was to systematically review the evidence relating neighborhood environment and obesity risk among urban, low socioeconomic status (SES) Black and Hispanic children. METHODS: We included studies published from 1993 through early 2017 from PubMed, SCOPUS, Web of Science, and Sociological Abstracts databases investigating relationships between empirically measured neighborhood characteristics and obesity risk factors in the populations of interest. Databases were last searched on May 8, 2018. Initial analysis took place during 2014 and was completed during 2017. We extracted data on study population, design, and associations between neighborhood characteristics and obesity risk factors. RESULTS: We identified 2011 unique studies; 24 were included. Few studies demonstrated consistent patterns of association. Most neighborhood characteristics were not examined across multiple studies. BMI may be related to living in a lower-income neighborhood or convenience store access. CONCLUSIONS: This review found that the body of evidence relating neighborhood exposures and obesity risk factors among urban, low SES Black (also commonly referred to in the literature as "non-Hispanic Black" or African American) and Hispanic children is limited. Given the high risk of obesity and cardiovascular disease among these populations throughout the life course, research on neighborhood determinants of obesity should specifically include these populations, ensuring adequate power and methodological rigor to detect differences.

Colchicine attenuates renal injury in a model of hypertensive chronic kidney disease.

Hypertension is a risk factor for chronic kidney disease, particularly when associated with impaired renal autoregulation and thereby increased intraglomerular pressure (Pgc). Elevated Pgc can be modeled in vitro by exposing glomerular mesangial cells to mechanical strain. We previously showed that RhoA mediates strain-induced matrix production. Here, we show that RhoA activation is dependent on an intact microtubule network. Upregulation of the profibrotic cytokine connective tissue growth factor (CTGF) by mechanical strain is dependent on RhoA activation and inhibited by microtubule disruption. We tested the effects of the microtubule depolymerizing agent colchicine in 5/6 nephrectomized rats, a model of chronic kidney disease driven by elevated Pgc. Colchicine inhibited glomerular RhoA activation and attenuated both glomerular sclerosis and interstitial fibrosis without affecting systemic blood pressure. Upregulation of the matrix proteins collagen I and fibronectin, as well as CTGF, was attenuated by colchicine. Activity of the profibrotic cytokine TGF-ß, as assessed by Smad3 phosphorylation, was also inhibited by colchicine. Microtubule disruption significantly decreased renal infiltration of lymphocytes and macrophages. Our studies thus indicate that colchicine modifies hypertensive renal fibrosis. Its protective effects are likely mediated by inhibition of RhoA signaling and renal infiltration of inflammatory cells. Already well-established in clinical practice for other indications, prevention of hypertension-associated renal fibrosis may represent a new potential use for colchicine.