'It is in our hands-Why wait until you are sick?': Perceptions about diabetes prevention of Latina mothers in Mexico and the United States.

AIMS: This study aimed to understand the perceptions driving type 2 diabetes mellitus prevention and management behaviours of Mexican and Latina mothers in Mexico and the United States. METHODS: Low-income Mexican mothers in San Luis Potosí, Mexico and Latina mothers in Illinois, United States, were recruited by the Holistic Obesity Prevention Study (HOPS). Verbatim transcripts of the semistructured interviews conducted in Spanish (n = 24) and English (n = 1) were analysed using the Health Belief Model (HBM) framework. RESULTS: Of the 25 participants, 22 (88%) indicated 'knowing someone with diabetes'-specifically a father (n = 8), mother (n = 6) or grandparent (n = 7). Using the HBM, themes showed that mothers perceived: that Type 2 diabetes can happen to anyone, are attributable to genetic predisposition and may be driven by strong emotions (perceived susceptibility). Type 2 diabetes introduces severe comorbidities and emotional difficulties for people and their families (perceived severity). Adopting a healthier diet, exercising and staying in good spirits were recognized as benefits of Type 2 diabetes prevention (perceived benefits). The costs of food, challenges of exercising, dieting, modifying habits and time limitations were recognized as perceived costs. Cues to action included doctors' recommendations (external) and fear (internal). Mothers acknowledged they could live a healthy life by controlling their weight, exercising, adhering to treatments/medications and having the determination to carry-on (self-efficacy). CONCLUSIONS: Mothers sought to prevent Type 2 diabetes and live healthy lives, particularly, after receiving a diagnosis of gestational diabetes or when learning about their children's risks for Type 2 diabetes but perceived significant barriers to Type 2 diabetes prevention.

Examining the Macrosystem Level of Influence on Community Health Worker Effectiveness in the State of Nebraska: A Qualitative Approach.

Community health workers (CHWs) serve as the linkage between community and providers and are stakeholders for bridging services to the public. However, integration of CHWs into health care organizations is often lacking. This study explored macrosystem level barriers faced by CHWs and their ability to do their jobs effectively. Using qualitative interviews from CHWs (n = 28) in Nebraska, we used an abductive approach to derive the following themes: (1) CHWs and client macrosystem barriers, (2) CHW workforce supports, and (3) macrosystem solutions for CHW workforce sustainability. Study results also found various macrosystem barriers affecting CHW workforces including immigration policies, insurance policies, funding sources, supervisor support, and obstacles for health seeking of clients. Moreover, through the lens of CHWs, results revealed the need to provide and advocate for solutions that prioritize the needs of CHWs as they continue to fill a crucial gap in community healthcare systems.

Dietary Iron Deficiency Modulates Adipocyte Iron Homeostasis, Adaptive Thermogenesis, and Obesity in C57BL/6 Mice.

BACKGROUND: Adaptive thermogenesis is an iron-demanding pathway, significantly contributing to whole-body energy expenditure. However, the effects of iron-deficient diets on adaptive thermogenesis and obesity remain unknown. OBJECTIVES: We aimed to determine the impact of dietary iron deficiency on iron homeostasis in adipocytes, adaptive thermogenic capacity, and metabolic consequences in obesity. METHODS: C57BL/6 male mice were assigned to either the iron-adequate (IA, 35 ppm) or the iron-deficient group (ID, 3 ppm) at weaning. Upon 8 wk of age, both IA and ID groups received an isocaloric high-fat diet (45% kcal from fat) for 10 wk, maintaining the same iron content. Mice (n = 8) were used to determine the iron status at the systemic and tissue levels and lipid metabolism and inflammatory signaling in adipose tissue. The same mice were used to evaluate cold tolerance (4°C) for 3 h. For assessing adaptive thermogenesis, mice (n = 5) received an intraperitoneal injection of ß3-adrenoceptor agonist CL316243 (CL) for 5 d. RESULTS: Compared with the IA group, the ID group had nonanemic iron deficiency, lower serum ferritin (42.8%, P < 0.01), and greater weight gain (8.67%, P < 0.05) and insulin resistance (159%, P < 0.01), partly due to reduced AMP-activated protein kinase activation (61.0%, P < 0.05). Upon cold exposure, the ID group maintained a core body temperature 2°C lower than the IA group. The ID group had lower iron content (47.0%, P < 0.01) in the inguinal adipose tissue (iWAT) than the IA group, which was associated with impaired adaptive thermogenesis. In response to CL, ID mice showed decreased heat production (P < 0.01) and defective upregulation of beige adipocyte-specific markers, including uncoupling protein 1 (41.1%, P < 0.001), transferrin receptor 1 (47.5%, P < 0.001), and mitochondrial respiratory chain complexes (P < 0.05) compared with IA mice. CONCLUSIONS: Dietary iron deficiency deregulates iron balance in the iWAT and impairs adaptive thermogenesis, thereby escalating the diet-induced weight gain in C57BL/6 mice.

Immunomodulatory Role of Urolithin A on Metabolic Diseases.

Urolithin A (UroA) is a gut metabolite produced from ellagic acid-containing foods such as pomegranates, berries, and walnuts. UroA is of growing interest due to its therapeutic potential for various metabolic diseases based on immunomodulatory properties. Recent advances in UroA research suggest that UroA administration attenuates inflammation in various tissues, including the brain, adipose, heart, and liver tissues, leading to the potential delay or prevention of the onset of Alzheimer's disease, type 2 diabetes mellitus, and non-alcoholic fatty liver disease. In this review, we focus on recent updates of the anti-inflammatory function of UroA and summarize the potential mechanisms by which UroA may help attenuate the onset of diseases in a tissue-specific manner. Therefore, this review aims to shed new insights into UroA as a potent anti-inflammatory molecule to prevent immunometabolic diseases, either by dietary intervention with ellagic acid-rich food or by UroA administration as a new pharmaceutical drug.

Differential Effects of Whole Red Raspberry Polyphenols and Their Gut Metabolite Urolithin A on Neuroinflammation in BV-2 Microglia.

Whole red raspberry polyphenols (RRW), including ellagic acid, and their gut-derived metabolite, urolithin A (UroA), attenuate inflammation and confer health benefits. Although results from recent studies indicate that polyphenols and UroA also provide neuroprotective effects, these compounds differ in their bioavailability and may, therefore, have unique effects on limiting neuroinflammation. Accordingly, we aimed to compare the neuroprotective effects of RRW and UroA on BV-2 microglia under both 3 h and 12 and 24 h inflammatory conditions. In inflammation induced by lipopolysaccharide (LPS) and ATP stimulation after 3 h, RRW and UroA suppressed pro-inflammatory cytokine gene expression and regulated the JNK/c-Jun signaling pathway. UroA also reduced inducible nitric oxide synthase gene expression and promoted M2 microglial polarization. During inflammatory conditions induced by either 12 or 24 h stimulation with LPS, UroA-but not RRW-dampened pro-inflammatory cytokine gene expression and suppressed JNK/c-Jun signaling. Taken together, these results demonstrate that RRW and its gut-derived metabolite UroA differentially regulate neuroprotective responses in microglia during 3 h versus 12 and 24 h inflammatory conditions.

Urolithin A, a Gut Metabolite, Improves Insulin Sensitivity Through Augmentation of Mitochondrial Function and Biogenesis.

OBJECTIVE: Urolithin A (UroA) is a major metabolite of ellagic acid produced following microbial catabolism in the gut. Emerging evidence has suggested that UroA modulates energy metabolism in various cells. However, UroA's physiological functions related to obesity and insulin resistance remain unclear. METHODS: Male mice were intraperitoneally administrated either UroA or dimethyl sulfoxide (vehicle) along with a high-fat diet for 12 weeks. Insulin sensitivity was evaluated via glucose and insulin tolerance tests and acute insulin signaling. The effects of UroA on hepatic triglyceride accumulation, adipocyte size, mitochondrial DNA content, and proinflammatory gene expressions were determined. The impact of UroA on macrophage polarization and mitochondrial respiration were assessed in bone marrow-derived macrophages. RESULTS: Administration of UroA (1) improved systemic insulin sensitivity, (2) attenuated triglyceride accumulation and elevated mitochondrial biogenesis in the liver, (3) reduced adipocyte hypertrophy and macrophage infiltration into the adipose tissue, and (4) altered M1/M2 polarization in peritoneal macrophages. In addition, UroA favored macrophage M2 polarization and mitochondrial respiration in bone marrow-derived macrophages. CONCLUSIONS: UroA plays a direct role in improving systemic insulin sensitivity independent of its parental compounds. This work supports UroA's role in the metabolic benefits of ellagic acid-rich foods and highlights the significance of its microbial transformation in the gut.

Maternal n-3 PUFA supplementation promotes fetal brown adipose tissue development through epigenetic modifications in C57BL/6 mice.

Brown adipose tissue (BAT) is a crucial regulator of energy expenditure. Emerging evidence suggests that n-3 PUFA potentiate brown adipogenesis in vitro. Since the pregnancy and lactation is a critical time for brown fat formation, we hypothesized that maternal supplementation of n-3 PUFA promotes BAT development in offspring. Female C57BL/6 mice were fed a diet containing n-3 PUFA (3%) derived from fish oil (FO), or an isocaloric diet devoid of n-3 PUFA (Cont) during pregnancy and lactation. Maternal n-3 PUFA intake was delivered to the BAT of neonates significantly reducing the n-6/n-3 ratio. The maternal n-3 PUFA exposure was linked with upregulated brown-specific gene and protein profiles and the functional cluster of brown-specific miRNAs. In addition, maternal n-3 PUFA induced histone modifications in the BAT evidenced by 1) increased epigenetic signature of brown adipogenesis, i.e., H3K27Ac and H3K9me2, 2) modified chromatin-remodeling enzymes, and 3) enriched the H3K27Ac in the promoter region of Ucp1. The offspring received maternal n-3 PUFA nutrition exhibited a significant increase in whole-body energy expenditure and better maintenance of core body temperature against acute cold treatment. Collectively, our results suggest that maternal n-3 PUFA supplementation potentiates fetal BAT development via the synergistic action of miRNA production and histone modifications, which may confer long-lasting metabolic benefits to offspring.