Obesity is a complex, chronic disease, frequently associated with multiple comorbidities. Its management is hampered by a lack of translation of evidence on chronicity and pathophysiology into clinical practice. Also, it is not well understood how to support effective provider-patient communication that adequately addresses patients' personal root causes and barriers and helps them feel capable to take action for their health. This study examined interpersonal processes during clinical consultations, their impacts, and outcomes with the aim to develop an approach to personalized obesity assessment and care planning. We used a qualitative, explorative design with 20 participants with obesity, sampling for maximum variation, to examine video-recorded consultations, patient interviews at three time points, provider interviews and patient journals. Analysis was grounded in a dialogic interactional perspective and found eight key processes that supported patients in making changes to improve health: compassion and listening; making sense of root causes and contextual factors in the patient's story; recognizing strengths; reframing misconceptions about obesity; focusing on whole-person health; action planning; fostering reflection and experimenting. Patient outcomes include activation, improved physical and psychological health. The proposed approach fosters emphatic care relationships and sensible care plans that support patients in making manageable changes to improve health.

This study examined whether physical activity (PA) mediated the relationships of four PA-related environmental settings (home, school, neighborhood environments and convenient facilities) with body mass index (BMI) among Chinese adolescents aged 13-18 years. Two setting indicators were assessed: (1) perceived availability of environmental resources and (2) perceived importance of environmental resources. Mediation analysis indicated that PA mediated the associations of perceived availability of the home environment, convenient facilities, and perceived importance of the school environment and BMI z-score with ratios of mediating to total effects of 46.2%, 37.1%, and 37.5% respectively. Findings suggest that PA is a mechanism by which several environmental correlates may affect adolescents' body weight.

Obesity results from an excessive expansion of white adipose tissue (WAT), which is still poorly understood from an etiologic-mechanistic perspective. Here, we report that Nck1, a Src homology domain-containing adaptor, is upregulated during WAT expansion and in vitro adipogenesis. In agreement, Nck1 mRNA correlates positively with peroxisome proliferator-activated receptor (PPAR) γ and adiponectin mRNAs in the WAT of obese humans, whereas Nck1-deficient mice display smaller WAT depots with reduced number of adipocyte precursors and accumulation of extracellular matrix. Furthermore, silencing Nck1 in 3T3-L1 preadipocytes increases the proliferation and expression of genes encoding collagen, whereas it decreases the expression of adipogenic markers and impairs adipogenesis. Silencing Nck1 in 3T3-L1 preadipocytes also promotes the expression of platelet-derived growth factor (PDGF)-A and platelet-derived growth factor receptor (PDGFR) α activation and signaling. Preventing PDGFRα activation using imatinib, or through PDGF-A or PDGFRα deficiency, inhibits collagen expression in Nck1-deficient preadipocytes. Finally, imatinib rescues differentiation of Nck1-deficient preadipocytes. Altogether, our findings reveal that Nck1 modulates WAT development through PDGFRα-dependent remodeling of preadipocytes.

Consumption of high fat diet (HFD) is associated with increased cardiovascular risk factors among elderly people. Aging and obesity induced-cardiac remodeling includes hypertrophy and fibrosis. Gelsolin (GSN) induces cardiac hypertrophy and TGF-β, a key cytokine, which induces fibrosis. The relationship between TGF-β and GSN in aging induced cardiac remodeling is still unknown. We evaluated the expressions of TGF-β and GSN in HFD fed 22 months old aging SD rats, followed by the administration of either probucol or alcalase potato protein hydrolysate (APPH). Western blotting and Masson trichrome staining showed that APPH (45 and 75 mg/kg/day) and probucol (500 mg/kg/day) treatments significantly reduced the aging and HFD-induced hypertrophy and fibrosis. Echocardiograph showed that the performance of the hearts was improved in APPH, and probucol treated HFD aging rats. Serum from all rats was collected and H9c2 cells were cultured with collected serums separately. The GSN dependent hypertrophy was inhibited with an exogenous TGF-β in H9c2 cells cultured in HFD+ APPH treated serum. Thus, we propose that along with its role in cardiac fibrosis, TGF-β also acts as an upstream activator of GSN dependent hypertrophy. Hence, TGF-β in serum could be a promising therapeutic target for cardiac remodeling in aging and/or obese subjects.