Obesity-related changes in adipose tissue leukocytes, in particular adipose tissue macrophages (ATMs) and dendritic cells (ATDCs), are implicated in metabolic inflammation, insulin resistance, and altered regulation of adipocyte function. We evaluated stromal cell and white adipose tissue (WAT) expansion dynamics with high fat diet (HFD) feeding for 3-56 days, quantifying ATMs, ATDCs, endothelial cells (ECs), and preadipocytes (PAs) in visceral epididymal WAT and subcutaneous inguinal WAT. To better understand mechanisms of the early response to obesity, we evaluated ATM proliferation and lipid accumulation. ATMs, ATDCs, and ECs increased with rapid WAT expansion, with ATMs derived primarily from a CCR2-independent resident population. WAT expansion stimulated proliferation in resident ATMs and ECs, but not CD11c ATMs or ATDCs. ATM proliferation was unperturbed in Csf2- and Rag1-deficient mice with WAT expansion. Additionally, ATM apoptosis decreased with WAT expansion, and proliferation and apoptosis reverted to baseline with weight loss. Adipocytes reached maximal hypertrophy at 28 days of HFD, coinciding with a plateau in resident ATM accumulation and the appearance of lipid-laden CD11c ATMs in visceral epididymal WAT. ATM increases were proportional to tissue expansion and adipocyte hypertrophy, supporting adipocyte-mediated regulation of resident ATMs. The appearance of lipid-laden CD11c ATMs at peak adipocyte size supports a role in responding to ectopic lipid accumulation within adipose tissue. In contrast, ATDCs increase independently of proliferation and may be derived from circulating precursors. These changes precede and establish the setting in which large-scale adipose tissue infiltration of CD11c ATMs, inflammation, and adipose tissue dysfunction contributes to insulin resistance.

Objective Weight regain after weight loss is common, and there is evidence to suggest negative effects on health because of weight cycling. This study sought to investigate the impact of weight regain in formerly obese mice on adipose tissue architecture and stromal cell function. Methods A diet‐switch model was employed for obesity induction, weight loss, and weight regain in mice. Flow cytometry quantified adipose tissue leukocytes in adipose tissue. Liver and adipose tissue depots were compared to determine tissue‐specific effects of weight cycling. Results Epididymal white adipose tissue of formerly obese mice failed to expand in response to repeat exposure to high‐fat diet and retained elevated numbers of macrophages and T cells. Weight regain was associated with disproportionally elevated liver mass, hepatic triglyceride content, serum insulin concentration, and serum transaminase concentration. These effects occurred despite an extended 6‐month weight loss cycle and they demonstrate that formerly obese mice maintain durable alterations in their physiological response to weight regain. Conditioned media from epididymal adipose tissue of formerly obese mice inhibited adipogenesis of 3T3‐L1 preadipocytes, suggesting a potential mechanism to explain failed epididymal adipose tissue expansion during weight regain. Conclusions Metabolic abnormalities related to defects in adipose tissue expansion and ongoing dysfunction manifest in formerly obese mice during weight regain.

Gestational diabetes mellitus (GDM) increases type 2 diabetes risk; however, postpartum diabetes screening rates are low. Using semi-structured interviews and focus groups, this study investigates the understanding of GDM and its relationship to future diabetes risk and diabetes prevention among patients with public or no insurance (n = 36), health care providers (n = 21), and clinic staff (n = 9) from Federally Qualified Health Centers. Five main themes emerged: 1) general understanding of GDM diagnosis with focus on neonatal complications; 2) variable recall of diet, exercise, and weight recommendations; 3) overwhelming medication and self-monitoring routines; 4) short-term focus of type 2 diabetes risk and screening; and 5) limited understanding of all options for diabetes prevention. The results may inform diabetes screening and prevention interventions in primary care settings.

Objective Gestational diabetes mellitus (GDM) is increasing in the United States, with higher rates among minoritized racial and ethnic populations and lower income populations. GDM increases risk for type 2 diabetes (T2DM), and postpartum diabetes screening and prevention are imperative. This qualitative study examines barriers and facilitators to postpartum T2DM screening and prevention among non-privately insured individuals with a history of GDM in a state prior to Medicaid expansion. Methods Thirty-six non-privately insured women with a history of GDM completed semi-structured interviews. Four focus groups and seven interviews were conducted with 30 nurse practitioners, physicians, physician assistants, nurses and registered dietitians from Federally Qualified Health Centers in St. Louis, MO. Interviews and focus groups were audio-recorded and transcribed. Data were analyzed using an integrative thematic analysis informed by the socio-ecological model. Results Barriers and facilitators to T2DM screening and prevention occur across multiple environments (society, healthcare system, interpersonal, and individual). Societal barriers include insurance issues, unemployment, and lack of transportation, childcare, safe housing, and healthy food access, while facilitators include government sponsored programs and community organizations. Healthcare system barriers include care fragmentation, scheduling policies and time constraints while facilitators include care coordination, pregnancy support groups, and education materials. Interpersonal barriers include negative care experiences, cultural differences, communication challenges, competing priorities, and lack of a social support network, while facilitators include family and friend support and positive care experiences. Individual barriers include health complications and unhealthy food and exercise patterns, while facilitators include child wellbeing, empowered attitudes and healthy food and exercise patterns. Conclusions The socioecological model highlights the societal and systemic determinants that encompass individual and interpersonal factors affecting postpartum T2DM screening and prevention. This framework can inform multi-level interventions to increase postpartum T2DM screening and prevention in this high-risk population, including policy changes to alleviate higher-level barriers.

Gestational diabetes mellitus (GDM) increases type 2 diabetes risk; however, postpartum diabetes screening rates are low. Using semi-structured interviews and focus groups, this study investigates the understanding of GDM and its relationship to future diabetes risk and diabetes prevention among patients with public or no insurance (<i>n </i>= 36), health care providers (<i>n </i>= 21), and clinic staff (<i>n </i>= 9) from Federally Qualified Health Centers. Five main themes emerged: <i>1</i>) general understanding of GDM diagnosis with focus on neonatal complications; <i>2</i>) variable recall of diet, exercise, and weight recommendations; <i>3</i>) overwhelming medication and self-monitoring routines; <i>4</i>) short-term focus of type 2 diabetes risk and screening; and <i>5</i>) limited understanding of all options for diabetes prevention. The results may inform diabetes screening and prevention interventions in primary care settings.