Association of neighborhood-level socioeconomic status and urban heat in China: Evidence from Hangzhou.

The escalating contradiction between global urban development and thermal environments has become increasingly apparent, underscoring the imperative to address social inequality in heat exposure and advocate for environmental justice (EJ) in the pursuit of sustainable urban development. To bridge the research gap in this domain, a comprehensive study was conducted to examine the correlation mechanism linking the thermal environment with the socioeconomic status (SES) of Chinese cities, employing Hangzhou as a representative case-a pivotal city among China's "four fire stoves". The investigation involved analyzing the spatial distribution pattern of diurnal Land Surface Temperature (LST) during the summer months spanning 2016 to 2018 (July to September). For SES characterization, a holistic indicator was established. Community-level LST variables were derived from LST surfaces obtained through the Terra and Aqua satellite MODIS sensors, with the community serving as the fundamental unit of analysis. The relationship between SES and LST was explored using random forest regression (RF), eXtreme Gradient Boosting (XGBoost), and support vector regression (SVR) to assess socioeconomic inequality in urban heat. The findings reveal that (1) RF exhibits the highest fitting accuracy and adeptly elucidates the nonlinear relationship and marginal effects between LST variables and SES. (2) Community SES in the Hangzhou metropolitan area exhibits spatial clustering. (3) Residents of low and middle SES communities experience heightened heat inequality. (4) A complex nonlinear relationship exists between daytime and nighttime LST and SES, with significant social disparities in urban heat within specific temperature thresholds. When deciding on measures to advance thermal environmental justice, it is crucial to prioritize both relatively disadvantaged groups and specific temperature intervals. This study departs from conventional approaches, exploring the nonlinear relationship between SES and urban heat at a fine scale, thereby assisting urban planners in developing effective strategies.

A POI and LST Adjusted NTL Urban Index for Urban Built-Up Area Extraction.

Nighttime light (NTL) images have been broadly applied to extract urban built-up areas in recent years. However, the typical NTL images provided by Defense Meteorological Satellite Program/Operational Linescan System (DMSP/OLS) and National Polar-Orbiting Partnership's Visible Infrared Imaging Radiometer Suite (NPP/VIIRS) have the drawbacks of low resolution and blooming effect, which bring difficulty for the application of them in urban built-up area extraction. Therefore, this paper proposes the POI (point of interest) and LST (land surface temperature) adjusted NTL urban index (PLANUI) to extract the urban built-up areas with high accuracy. PLANUI is the first urban index to integrate POI and NTL for urban built-up area extraction. In this paper, NPP/VIIRS and Luojia 1-01 images were introduced as the original NTL data and the vegetation adjusted NTL urban index (VANUI) was selected as the comparison item. The threshold method was utilized to extract urban built-up areas from these data. The results show that: (1) Based on the comparison with the reference data, the PLANUI can make up the shortcoming of low resolution and the blooming effect of NTL effectively. (2) Compared with the VANUI, the PLANUI can significantly improve the accuracy of the urban built-up areas extracted and characterize urban features. (3) According to the results based on NPP/VIIRS and Luojia 1-01 images, the PLANUI has extensive applicability, both for regions with different degrees of economic development and NTL data with different resolutions. PLANUI can enhance the features of urban built-up areas with social sensing data and natural remote sensing data, which helps to weaken the NTL blooming effect and improve the extraction accuracy. PLANUI can provide an effective approach for urban built-up area extraction, which plays a certain guiding role for the study of urban structure, urban expansion, and urban planning and governance.

Association of betatrophin with metabolic characteristics in overweight/obese and lean women with PCOS.

As a new hormone, betatrophin has gained attention as a potential new target to combat insulin resistance (IR) and diabetes. Polycystic ovary syndrome (PCOS) is a common endocrine and metabolic disorder among women of the reproductive age with long term sequelae which include IR and metabolic syndrome. The aim of this study is to evaluate the circulating plasma betatrophin levels in overweight/obese or lean women with or without PCOS and also to elucidate possible correlations with anthropometric and metabolic parameters. Thirty-two patients with PCOS as well as fifty-three control subjects were enrolled after obtaining informed written consent. Clinical and biochemical parameters of all subjects were determined. Plasma adiponectin, GLP-1 and betatrophin levels were measured by ELISA. Plasma betatrophin levels were significantly increased in lean patients with PCOS compared with lean and obese controls. Moreover, in PCOS group, betatrophin levels were significantly negatively correlated with waist hip ratio (WHR), fasting insulin level (FINS) and HOMA-IR, whereas, significantly positively correlated with adiponectin level. Multiple regression analysis showed that HOMA-IR was an independent factor influencing serum betatrophin levels. Further follow-up studies are needed to highlight whether and how increased betatrophin secretion play an important role in IR and carbohydrates metabolism in patients with PCOS.

Gender Disparity in the Relationship between Prevalence of Thyroid Nodules and Metabolic Syndrome Components: The SHDC-CDPC Community-Based Study.

The study is aimed to investigate the pathogenesis underlying the increased prevalence of thyroid nodule (TN) in different levels of metabolic syndrome (MetS) components and analyze the relationships between TN and MetS components. A total of 6,798 subjects, including 2201 patients with TN, were enrolled in this study. Anthropometric, biochemical, thyroid ultrasonographic, and other metabolic parameters were all measured. There was obviously sexual difference in the prevalence of TN (males 26.0%, females 38.5%, resp.). The prevalence of TN in hyperuricemia (45.7% versus 37.4%, P = 0.001), NAFLD (41.2% versus 36.4%, P < 0.05), and MetS (41.4% versus 35.4%, P < 0.001) groups was significantly increased only in females. Insulin resistance [OR = 1.31 (1.15, 1.49)], MetS [OR = 1.18 (1.03, 1.35)], and diabetes [OR = 1.25 (1.06, 1.48)] were all independent risk factors for TN in total subjects, whereas, after stratified analysis of gender, MetS [OR = 1.29, (1.09, 1.53)] and diabetes [OR = 1.47, (1.17, 1.84)] are still strongly and independently associated with the higher risks of TN in female subjects, but not in males. Our results suggest that the components of MetS might associate with the higher risks of TN in women than in men, but further cohort study of this gender disparity in the association between TN and MetS is required.

Interferon regulatory factors are transcriptional regulators of adipogenesis.

We have sought to identify transcriptional pathways in adipogenesis using an integrated experimental and computational approach. Here, we employ high-throughput DNase hypersensitivity analysis to find regions of altered chromatin structure surrounding key adipocyte genes. Regions that display differentiation-dependent changes in hypersensitivity were used to predict binding sites for proteins involved in adipogenesis. A high-scoring example was a binding motif for interferon regulatory factor (IRF) family members. Expression of all nine mammalian IRF mRNAs is regulated during adipogenesis, and several bind to the identified motifs in a differentiation-dependent manner. Furthermore, several IRF proteins repress differentiation. This analysis suggests an important role for IRF proteins in adipocyte biology and demonstrates the utility of this approach in identifying cis- and trans-acting factors not previously suspected to participate in adipogenesis.

A role for long-chain acyl-CoA synthetase-4 (ACSL4) in diet-induced phospholipid remodeling and obesity-associated adipocyte dysfunction.

OBJECTIVE: Regulation of fatty acid (FA) metabolism is central to adipocyte dysfunction during diet-induced obesity (DIO). Long-chain acyl-CoA synthetase-4 (ACSL4) has been hypothesized to modulate the metabolic fates of polyunsaturated FA (PUFA), including arachidonic acid (AA), but the in vivo actions of ACSL4 are unknown. The purpose of our studies was to determine the in vivo role of adipocyte ACSL4 in regulating obesity-associated adipocyte dysfunction. METHODS: We developed a novel mouse model with adipocyte-specific ablation of ACSL4 (Ad-KO) using loxP Cre recombinase technology. Metabolic phenotyping of Ad-KO mice relative to their floxed littermates (ACSL4floxed) was performed, including body weight and body composition over time; insulin and glucose tolerance tests; and energy expenditure, activity, and food intake in metabolic cages. Adipocytes were isolated for ex vivo adipocyte oxygen consumption by Clark electrode and lipidomics analysis. In vitro adipocyte analysis including oxygen consumption by Seahorse and real-time PCR analysis were performed to confirm our in vivo findings. RESULTS: Ad-KO mice were protected against DIO, adipocyte death, and metabolic dysfunction. Adipocytes from Ad-KO mice fed high-fat diet (HFD) had reduced incorporation of AA into phospholipids (PL), free AA, and levels of the AA lipid peroxidation product 4-hydroxynonenal (4-HNE). Additionally, adipocytes from Ad-KO mice fed HFD had reduced p53 activation and increased adipocyte oxygen consumption (OCR), which we demonstrated are direct effects of 4-HNE on adipocytes in vitro. CONCLUSION: These studies are the first to elucidate ACSL4's in vivo actions to regulate the incorporation of AA into PL and downstream effects on DIO-associated adipocyte dysfunction. By reducing the incorporation of AA into PL and free fatty acid pools in adipocytes, Ad-KO mice were significantly protected against HFD-induced increases in adipose and liver fat accumulation, adipocyte death, gonadal white adipose tissue (gWAT) inflammation, and insulin resistance (IR). Additionally, deficiency of adipocyte ACSL4 expression in mice fed a HFD resulted in increased gWAT adipocyte OCR and whole body energy expenditure (EE).

Nonalcoholic Fatty Liver Disease and Associated Metabolic Risks of Hypertension in Type 2 Diabetes: A Cross-Sectional Community-Based Study.

The mechanisms facilitating hypertension in diabetes still remain to be elucidated. Nonalcoholic fatty liver disease (NAFLD), which is a higher risk factor for insulin resistance, shares many predisposing factors with diabetes. However, little work has been performed on the pathogenesis of hypertension in type 2 diabetes (T2DM) with NAFLD. The aim of this study is to investigate the prevalence of hypertension in different glycemic statuses and to analyze relationships between NAFLD, metabolic risks, and hypertension within a large community-based population after informed written consent. A total of 9473 subjects aged over 45 years, including 1648 patients with T2DM, were enrolled in this cross-sectional study. Clinical and biochemical parameters of all participants were determined. The results suggested that the patients with prediabetes or T2DM were with higher risks to have hypertension. T2DM with NAFLD had significantly higher levels of blood pressure, triglyceride, uric acid, and HOMA-IR than those without NAFLD. Data analyses suggested that hypertriglyceridemia [OR = 1.773 (1.396, 2.251)], NAFLD [OR = 2.344 (1.736, 3.165)], hyperuricemia [OR = 1.474 (1.079, 2.012)], and insulin resistance [OR = 1.948 (1.540, 2.465)] were associated with the higher prevalence of hypertension independent of other metabolic risk factors in type 2 diabetes. Further studies are needed to focus on these associations.

MZF1 possesses a repressively regulatory function in ERCC1 expression.

ERCC1 is a critical gene within the nucleotide excision repair pathway. Overexpression of ERCC1 through promoter-mediating transcriptional regulation is associated with repair of cisplatin-induced DNA damage and clinical resistance to platinum-chemotherapy. Several transcriptional repressors and activators within the 5'-flanking region of the ERCC1 gene may be involved in the up-regulation of this gene. Minimal sequence within the promoter region required for ERCC1 transcription was analyzed by CAT assay and demonstrated that the region of -220 to -110 is essential to constitutive expression of ERCC1 gene in ovarian cancer cell line A2780/CP70. A more forward upstream region seems to be responsible for cisplatin-induced expression. Study of the functional cis-element in this region by electrophoretic mobility shift assay indicates that a MZF1-like site as well as an AP1-like site responded in a time-dependent manner to cisplatin stimulation with altered binding activities. EMSA with MZF1 ZN1-4 consensus oligonucleotides suggests that the MZF1 N-terminal domain of zinc finger cluster may bind to the MZF1-like site of the ERCC1 promoter region. MZF1 mRNA in A2780/CP70 cells decreased upon cisplatin exposure as analyzed by quantitative PCR, suggesting that MZF1 may mediate cisplatin-invoked gene expression in these cells. Overexpression of MZF1 repressed the ERCC1 promoter activity as determined in co-transfection assay, suggesting that MZF1 might be a repressor of ERCC1 transcription upon cisplatin exposure. In summary, our studies revealed a core promoter region and adjacent drug-responsible region within the ERCC1 promoter. The drug-responsible region contains cis-elements of activator, AP1 and repressor, MZF1. In response to cisplatin treatment, decreased MZF1 and increased AP1 binding activities appear to be the leading mechanism of up-regulation of ERCC1 expression. Our findings imply potential therapeutic strategies to antagonize drug resistant mechanisms in treatment of human ovarian cancer.

AVP (4-8) May Stimulate a G Protein-coupled Receptor in Rat Hippocampal Synaptosomal Membranes.

As a metabolite of arginine-vasopressin, AVP(4-8) has been shown to have potent memory-enhancing activity and to induce a series of physiological and biochemical events in rat brain. GTP-binding protein is known to be a revolving stage of transmembrane signal transduction to mediate physiochemical responses of neurotransmitters and neuromodulators. A specific binding site of AVP(4-8) in the rat hippocampal synaptic membranes was identified by radio-receptor assay and after binding to membranes, AVP(4-8) enhanced the binding of Guanosine -5'-O-(3-[(35)S]thio)triphosphate ([(35)S]GTPgammaS), and this enhancement could be completely reversed by the antagonist of AVP(4-8), ZNC(C)PR. Based on the alone results, we suggest that AVP(4-8) exerts its function as neurotransmitter through a G-protein-coupled receptor on the synaptosomal membrane of rat hippocampus.

The Binding Sites of AVP(4-8) in Rat Brain Are Different from the Known Receptors.

No Abstract

The role of lipid droplets in metabolic disease in rodents and humans.

Lipid droplets (LDs) are intracellular organelles that store neutral lipids within cells. Over the last two decades there has been a dramatic growth in our understanding of LD biology and, in parallel, our understanding of the role of LDs in health and disease. In its simplest form, the LD regulates the storage and hydrolysis of neutral lipids, including triacylglycerol and/or cholesterol esters. It is becoming increasingly evident that alterations in the regulation of LD physiology and metabolism influence the risk of developing metabolic diseases such as diabetes. In this review we provide an update on the role of LD-associated proteins and LDs in metabolic disease.

The adipokine lipocalin 2 is regulated by obesity and promotes insulin resistance.

OBJECTIVE: We identified lipocalin 2 (Lcn2) as a gene induced by dexamethasone and tumor necrosis factor-alpha in cultured adipocytes. The purpose of this study was to determine how expression of Lcn2 is regulated in fat cells and to ascertain whether Lcn2 could be involved in metabolic dysregulation associated with obesity. RESEARCH DESIGN AND METHODS: We examined Lcn2 expression in murine tissues and in 3T3-L1 adipocytes in the presence and absence of various stimuli. We used quantitative Western blotting to observe Lcn2 serum levels in lean and obese mouse models. To assess effects on insulin action, we used retroviral delivery of short hairpin RNA to reduce Lcn2 levels in 3T3-L1 adipocytes. RESULTS: Lcn2 is highly expressed by fat cells in vivo and in vitro. Expression of Lcn2 is elevated by agents that promote insulin resistance and is reduced by thiazolidinediones. The expression of Lcn2 is induced during 3T3-L1 adipogenesis in a CCAAT/enhancer-binding protein-dependent manner. Lcn2 serum levels are elevated in multiple rodent models of obesity, and forced reduction of Lcn2 in 3T3-L1 adipocytes improves insulin action. Exogenous Lcn2 promotes insulin resistance in cultured hepatocytes. CONCLUSIONS: Lcn2 is an adipokine with potential importance in insulin resistance associated with obesity.