Obesity-related Hypertension Research Articles

Effects of BET Inhibition on lung micro-environmental changes in obesity-related pulmonary Arterial Hypertension (PAH)

Abstract Background Obesity is emerging as a pivotal risk factor for pulmonary arterial hypertension (PAH) but the underlying molecular mechanisms are poorly explored. The lung microenvironment, namely the cell-cell communication among fibroblasts, immune and endothelial cells, may significantly impact on vascular structure and function thus promoting microvascular disease in this setting. Obesity-induced chromatin modifications lead to maladaptive transcriptional programs altering cell function in different organs. Apabetalone (APA), a selective inhibitor of bromodomain and extra-terminal containing protein family (BET) proteins, prevents bromodomain-containing protein 4 (BRD4) interactions with chromatin thus modulating gene expression. Purpose To determine whether a new epi-drug, namely APA, affects the lung microenvironment in obesity-related PAH. Methods Mice were fed a normal diet (ND, control) or high-fat-diet (HFD) and L-NAME for 15 weeks to induce obesity-related PAH (obPAH). Echocardiography was performed. Pathways regulating obPAH were identified by single-cell nuclei RNA sequencing in lung specimens. Primary endothelial cells (ECs) and Fibroblasts (mFs) were freshly isolated from obPAH lungs and treated with APA for 48 hours. Cells and lung samples were used for molecular biology and histology. Cellular migration was investigated by in vitro gap closure. Results Obese mice displayed PAH as shown by increased pulmonary artery (PA) pressure, PA resistance, right ventricular wall thickness and reduced PA acceleration time. Of note, chronic APA treatment prevented PAH-related features in obese mice. To determine the cell types affected by APA, we performed scRNAseq. We found that fibroblast and endothelial cells had the highest enrichment of genes whose expression significantly correlated with echo-determined PAH features. ECs and mFs from obese mice displayed an altered phenotype whereas treatment with APA rescued obesity-driven ECs and mFs dysfunction. In obPAH ECs, we found increased expression of NF-kB p65-related inflammatory genes (IL-1β, IL-6, TNF-alpha) as well as enhanced p53 signaling. Moreover, obPAH-ECs expressed high levels of hypoxia-inducible factor (HIF1-α) and NADPH-oxidase-NOX4 with subsequent increase in ROS generation. Furthermore, APA treatment protected against cellular inflammation, senescence and oxidative stress. To evaluate the effect of APA and the paracrine response of fibroblasts, we performed a scratch assay on control mFs exposed to TGF-β or conditioned media collected from obPAH-ECs with and without APA. In both experimental settings, APA affected gap closure, suggesting that the treatment influences fibroblast migration through both a direct effect and paracrine mechanisms. Conclusions APA is able to reset the lung micro-envirnment in obesity thus reducing inflammation and senescence. BET inhibitors could represent potential therapeutic approaches in this setting.

Rising Prevalence of Obesity and Primary Hyperaldosteronism: Co-incidence or Connected Circumstances Leading to Hypertension? A Narrative Review.

While obesity and its associated complications, mainly diabetes and hypertension, have been the largest public health problems of modern world, the emerging data suggests an increasing prevalence of primary hyperaldosteronism (PA) as one of the most common undiagnosed causes of hypertension. We believe that rising prevalence of PA in the era of high rates of obesity is likely not a chance finding but is deeply intersected with the rising rates of obesity. Higher serum aldosterone concentrations and urinary aldosterone excretion have been observed in patients with increased body mass index or larger waist circumference. The in vitro and pre-clinical studies suggest that adipocytes not only synthesize and secrete aldosterone but also release factors which stimulate production of aldosterone from adrenal glands. Aldosterone excess causing ligand-dependent activation of the mineralocorticoid receptor (MR) has increasingly been recognized as one of the important mechanisms of obesity-related hypertension. The aldosterone excess in these cases can be labelled as acquired hyperaldosteronism to differentiate it from the non-obesity related classical cases of PA. Because of serious consequences, recognizing aldosterone excess in obesity is important, as it gives a more compelling reason for weight loss and guidance to choosing pharmacotherapy wisely. Dietary sodium restriction and mineralocorticoid receptor antagonists play important roles in the management of PA associated with obesity.

Impact of metabolic bariatric surgery on outcomes and the 10-year risk of major adverse cardiovascular events during a 7-year period: a retrospective cohort study.

Metabolic bariatric surgery offers enduring weight reduction and alleviation of obesity-related comorbidities, including dyslipidemia, diabetes, hypertension, and major adverse cardiovascular events (MACE). Long-term data on one-anastomosis gastric bypass (OAGB) and single-anastomosis duodenal-jejunal bypass with sleeve gastrectomy (SADJB-SG) is lacking, necessitating this investigation. In this multicenter prospectively-collected retrospective observational study, 830 adult Taiwanese patients (682 OAGB, 148 SADJB-SG) who underwent surgery from 1 January 2011 to 31 December 2017, were initially identified. Following protocol, 224 patients (177 OAGB, 47 SADJB-SG) with complete follow-up data at various intervals up to 3 years after surgery were included in the final analysis. The study's primary focus is to evaluate the long-term safety, efficacy, and durability of OAGB and SADJB-SG in promoting weight loss and diabetes remission. Additionally, changes in 10-year and lifetime risks of MACE before and 3-year after surgery are assessed using Taiwan MACE risk prediction model and the China-PAR project model. SADJB-SG patients exhibit higher diabetes prevalence, lower BMI, and more severe diabetes compared to OAGB. Both groups demonstrate significant improvements in BMI, diabetes, hypertension, and dyslipidemia three years after surgery, with the most substantial improvements occurring in the second year. The Taiwan MACE risk model reveals a significant reduction in 10-year MACE and stroke risks for both groups. The China-PAR project model indicates a synchronized reduction in atherosclerotic cardiovascular disease 10-year and lifetime risk in both OAGB and SADJB-SG groups. OAGB and SADJB-SG exhibit sustained improvements in weight reduction and obesity-related comorbidities over 3 years after surgery. Notably, both procedures contribute to a substantial reduction in 10-year MACE, stroke, and atherosclerotic cardiovascular disease risks. These findings underscore the efficacy of OAGB and SADJB-SG in the context of metabolic bariatric surgery.

Abstract MP08: Long-Term Impact of Bariatric Surgery on Hypertension Control and Remission: A Meta-Analysis of Randomized Controlled Trials

Background: Bariatric surgery is widely recognized as a highly effective intervention for addressing obesity and its associated metabolic complications. However, there is a paucity of evidence from randomized controlled trials (RCTs) with primary endpoints focusing on its impact on hypertension. Objective: We aimed to synthesize findings from pivotal RCTs until May 2024 to evaluate the long-term effects of bariatric surgery on hypertension in obese individuals compared to medical or lifestyle management. Methods: We analyzed data using RevMan 5.4 with a random effects model, employing the inverse variance method to report outcomes as risk ratios (RR) or weighted mean differences (WMD) with 95% confidence intervals (CI). Our study protocol is registered in PROSPERO (CRD42024527369). Results: The study comprised 18 RCTs involving 1386 obese patients (62.7% women) with a mean BMI of 38 kg/m 2 and an average follow-up duration of 1 to 5 years. On pooled analysis, there was a statistically significant difference in the rate of hypertension remission between patients who underwent bariatric surgery versus patients on medical/lifestyle management with an RR of 2.77 (95% CI: 1.26 to 6.10, p = 0.01). Additionally, a substantial reduction in the use of antihypertensive medications while maintaining controlled blood pressure was observed (RR: 7.10; 95% CI: 4.38 to 11.51, p < 0.00001), with no heterogeneity. Bariatric surgery also significantly improved systolic blood pressure control (WMD: -3.67; 95% CI: -5.53 to -1.80, p = 0.0001). Conclusion: Bariatric surgery emerges as a durable solution for obesity-related hypertension, offering remission and control of hypertension while reducing the dependence on antihypertensive medications.

Dietary apigenin ameliorates obesity-related hypertension through TRPV4-dependent vasorelaxation and TRPV4-independent adiponectin secretion

BackgroundObesity-related hypertension is a major cardiovascular risk factor. Apigenin, a natural flavonoid in celery, induces vascular dilation via endothelial transient receptor potential channel vanilla 4 (TRPV4) channels. This study aimed to explore apigenin's potential to alleviate obesity-related hypertension in mice and its underlying mechanisms. MethodsThe C57BL/6 and TRPV4 knockout mice were fed a high-fat diet and subjected to dietary intervention with apigenin. Body weight and tail blood pressure of the mice were measured during the feeding. Vascular reactivity was assessed through a DMT wire myograph systems in vitro. The distribution and expression of adiponectin and pro-inflammatory markers in brown fat were detected. Injecting adeno-associated eight (AAV8) viruses into brown adipose tissue (BAT) to determine whether adiponectin is indispensable for the therapeutic effect of apigenin. Palmitic acid (PA) was used in mouse brown adipocytes to examine the detailed mechanisms regulating adiponectin secretion. ResultsApigenin improved vasodilation and reduced blood pressure in obese mice, effects partly blocked in TRPV4 knockout. It also reduced weight gain independently of TRPV4. Apigenin increased adiponectin secretion from BAT; knockdown of adiponectin weakened its benefits. Apigenin downregulated Cluster of differentiation 38 (CD38), restoring Nicotinamide adenine dinucleotide+ (NAD+) levels and activating the NAD+/Sirtuin 1 (SIRT1) pathway, enhancing adiponectin expression. ConclusionsOur study indicates that dietary apigenin is suitable as a nonpharmaceutical intervention for obesity-related hypertension. In mechanism, in addition to improving vascular relaxation through the activation of endothelial TRPV4 channels, apigenin also directly alleviated adipose inflammation and increased adiponectin levels by inhibiting CD38.

The Analysis Study of Obesity-related hypertension and chronic kidney disease : A Comprehensive Systematic Review and Metaanalysis Study

The Analysis Study of Obesity-related hypertension and chronic kidney disease : A Comprehensive Systematic Review and Metaanalysis Study

Effect of adrenomedullin on obesity-related hypertension.

Effect of adrenomedullin on obesity-related hypertension.

Adrenomedullin improved endothelial dysfunction via receptor-Akt pathway in rats with obesity-related hypertension.

Obesity-related hypertension (OH) is accompanied by obvious endothelial dysfunction, which contributes to increased peripheral vascular resistance and hypertension. Adrenomedullin (ADM), a multifunctional active peptide, is elevated in obese humans. The OH rats induced by high fat diet (HFD) for 28 weeks and the human umbilical vein endothelial cells (HUVECs)-treated by palmitic acid (PA) were used to investigate the effects of ADM on endothelial dysfunction and the underlying mechanisms. Vascular reactivity was assessed using mesenteric arteriole rings, and the protein expression levels were examined by Western blot analysis. Compared with the control rats, OH rats exhibited hypertension and endothelial dysfunction, along with reduced eNOS protein expression and Akt activation, and increased protein expression of proinflammatory cytokines and ROS levels. Four-week ADM administration improved hypertension and endothelial function, increased eNOS protein expression and Akt activation, and attenuated endothelial inflammation and oxidative stress in OH rats. In vitro experiment, the antagonism of ADM receptors with ADM22-52 and the suppression of Akt signaling with A6730 significantly blocked ADM-caused increase of NO content and activation of eNOS and Akt, and inhibited the anti-inflammatory and anti-oxidant effect of ADM in PA-stimulated HUVECs. These data indicate that endothelial dysfunction in OH rats is partially attributable to the decreased NO level, and the increased inflammation and oxidative stress. ADM improves endothelial function and exerts hypotensive effect depending on the increase of NO, and its anti-inflammatory and anti-oxidant effect via receptor-Akt pathway.

A comparative study of carotid body chemosensitivity in lean and obese mice: Implication for obesity induced hypertension

Obesity is associated with increased circulating level of the hormone leptin. Previously we have shown in mice that, leptin induces hypertension acting on transient receptor potential melastatin 7 (Trpm7) channels in the carotid body (CB), a multi-modal peripheral chemoreceptor organ that controls breathing and drives sympathetic tone. Further, in mice leptin augments hypoxic ventilatory response which is abolished by CB denervation. This suggests a potential involvement of CB chemosensitivity. However, no comparative study of CB chemosensory responses has been conducted in lean and obese mice to support this notion. Based on these premises, we hypothesize that obese mice should have higher leptin induced CB chemosensory responses during normoxia and hypoxia compared to lean mice, and Trpm7 receptor antagonist should abolish/reduce these responses. To prove this, we measured afferent carotid sinus nerve (CSN) activity, using a novel ex vivo perfused mouse (male) CB preparation from lean (b.w.; 35 ± 0.5 gm) and diet induced obese (DIO) mice (b.w.; 53 ± 1.5gm) with C57BL/6J background. We found that compared to lean mice; (a) CSN response to hypoxia (PO2 =60 Torr) was 50% more in obese mice, (b) in presence of leptin (50nM), CSN responses to normoxia (PO2=100Torr) and hypoxia were augmented 50% and 150% more respectively in obese mice. Finally, leptin induced increase in CSN responses were partially reduced by Trpm7 antagonist FTY720 (3μM) in obese compared to lean mice. In conclusion, CB chemosensitivity is enhanced in obese compared to lean mice and CB Trpm7 channel could be a therapeutic target for obesity related hypertension. Grant support: NIH R01 HL1331000. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Reevaluating Adiponectin’s impact on obesity hypertension: a Chinese case-control study

BackgroundObesity and hypertension are major risk factors for cardiovascular diseases that affect millions of people worldwide. Both conditions are associated with chronic low-grade inflammation, which is mediated by adipokines such as adiponectin. Adiponectin is the most abundant adipokine that has a beneficial impact on metabolic and vascular biology, while high serum concentrations are associated with some syndromes. This “adiponectin paradox” still needs to be clarified in obesity-associated hypertension. The aim of this study was to investigate how adiponectin affects blood pressure, inflammation, and metabolic function in obesity hypertension using a Chinese adult case-control study.MethodsA case-control study that had finished recruiting 153 subjects divided as four characteristic groups. Adiponectin serum levels were tested by ELISA in these subjects among these four characteristic Chinese adult physical examination groups. Waist circumference (WC), body mass index (BMI), systolic blood pressure (SB), diastolic blood pressure (DB), and other clinical laboratory data were collected. Analyzation of correlations between the research index and differences between groups was done by SPSS.ResultsSerum adiponectin levels in the| normal healthy group (NH group) were significantly higher than those in the newly diagnosed untreated just-obesity group (JO group), and negatively correlated with the visceral adiposity index. With multiple linear egression analysis, it was found that, for serum adiponectin, gender, serum albumin (ALB), alanine aminotransferase (ALT) and high-density lipoprotein cholesterol (HDLC) were the significant independent correlates, and for SB, age and HDLC were the significant independent correlates, and for DB, alkaline phosphatase (ALP) was the significant independent correlate. The other variables did not reach significance in the model.ConclusionsOur study reveals that adiponectin’s role in obesity-hypertension is multifaceted and is influenced by the systemic metabolic homeostasis signaling axis. In obesity-related hypertension, compensatory effects, adiponectin resistance, and reduced adiponectin clearance from impaired kidneys and liver all contribute to the “adiponectin paradox”.

Chronic exercise improves renal AT1 and ETB receptor functions via modulating GRK4 expression in obese Zucker rats

ABSTRACT Background Physical activity has profound benefits on health, especially in patients with cardiovascular and metabolic disease. Exercise training can reduce oxidative stress, improve renal function, and thus lower blood pressure. However, the effect of exercise training on angiotensin II type 1 receptors (AT1R) and endothelin subtype B receptors (ETBR)-mediated diuresis and natriuresis in obese Zucker rats is unclear. Methods Lean and obese Zucker rats were exercised or placed on a nonmoving treadmill for 8 weeks. Blood pressure was measured by tail-cuff plethysmography, and functions of AT1R and ETBR in the kidney were measured by natriuresis, respectively. Results Our data showed that exercise training improved glucose and lipid metabolism, renal function and sodium excretion in obese Zucker rats, accompanied by decreased oxidative stress and GRK4 expression in obese Zucker rats. Moreover, exercise training reduced the Candesartan-induced an increase in diuresis and natriuresis and increased ETBR agonists (BQ3020)-mediated diuresis and natriuresis in obese Zucker rats, which were associated with decreased renal AT1R expression and ETBR phosphorylation levels. Conclusions The results demonstrate that exercise training lowers blood pressure via improving renal AT1R and ETBR function through modulating GRK4 expression in Obese Zucker Rats and provides potentially effective targets for obesity-related hypertension.

Accuracy and Performance of Triage Blood Pressure Measurements in A Real-World Clinic Setting

ObjectivesTo investigate the agreement and accuracy of triage blood pressure (BP) in a real-world clinic setting, compared with the reference standard. Study designPaired triage and standardized BP measurements from patients 4 through 21 years old evaluated in an obesity-related hypertension clinic were obtained via chart-review. Triage BPs were measured by a medical assistant or nurse, often by automated device. Triplicate manual BPs were obtained by the clinic physician. Bland-Altman analyses determined mean differences between paired triage and mean standardized BPs. GEE-based multivariable relative risk (RR) regression determined the RR of triage BP overestimation by ≥5mmHg. Overall agreement, sensitivity, specificity, positive predictive value, and negative predictive value of triage BP measurements identifying hypertensive BP were determined. Results130 participants with 347 clinic encounters were included. Mean age was 13.3 years (standard deviation 3.94), 76% were Black, and 58% were male. Overall mean systolic and diastolic BP difference was 8.7 mmHg (95% limits on agreement: -16.66, 34.07) and 4.1 mmHg (95% limits on agreement: -18.56, 26.68), respectively. Triage systolic BP was more likely overestimated by ≥5 mmHg when a large adult (RR=1.49; 95%CI: 1.00, 2.21) or thigh cuff (RR=1.94; 95%CI: 1.08, 3.51) was required compared with when a child/adult cuff was required. Overall agreement in identifying hypertensive BP was 57.6%. Sensitivity (52.6%), specificity (63.4%), positive predictive value (60.8%), and negative predictive value (55.3%) were low across all cuffs. ConclusionsThere was poor agreement between usual triage and standardized BP measurements, with potential for significant clinical implications.

Predictors of Cardiac Autonomic Dysfunction in Obesity-Related Hypertension.

Cardiac Autonomic Dysfunction (CAD) is an overlooked cardiovascular risk factor in individuals with obesity-related hypertension. Despite its clinical significance, there is a notable lack of clarity regarding the pathophysiological correlates involved in its onset and progression. The present study aimed to identify potential predictors of CAD in obesity-related hypertension. A total of 72 participants (34 men and 38 women) were enrolled. Comprehensive evaluations were conducted, including cardiac autonomic function assessments, body composition estimation and biochemical analysis. Participants were categorized as CAD-positive or CAD-negative based on Ewing's criteria for autonomic dysfunction. Univariate logistic regression analysis was performed to identify potential predictors for CAD. Multivariate logistic regression models were further constructed by adjusting clinically relevant covariates to identify independent predictors of CAD. Multivariate logistic regression analysis revealed that resting heart rate (HRrest), (odds ratio, confidence interval: 0.85, 0.78-0.93; p = 0.001) and percentage body fat (BF%), (odds ratio, confidence interval: 0.78, 0.64-0.96; p = 0.018) were significant independent predictors of CAD. Receiver Operating Characteristic curve analysis depicted optimal cut-off values for HRrest and BF% as >74.1bpm and >33.6%, respectively. Multicolinearity analysis showed variance inflation factors (VIF) below the cautionary threshold of 3. The HRrest and BF% emerged as significant independent predictors of CAD in obesity-related hypertension. Therapeutic strategies should target HRrest<74.1bpm and BF% <33.6% to mitigate CAD risk in this population. Future trials are required to establish causal relationships and may consider additional confounding variables in obesity-related hypertension.

Pannexin-3 stabilizes the transcription factor Bcl6 in a channel-independent manner to protect against vascular oxidative stress.

Targeted degradation regulates the activity of the transcriptional repressor Bcl6 and its ability to suppress oxidative stress and inflammation. Here, we report that abundance of endothelial Bcl6 is determined by its interaction with Golgi-localized pannexin 3 (Panx3) and that Bcl6 transcriptional activity protects against vascular oxidative stress. Consistent with data from obese, hypertensive humans, mice with an endothelial cell-specific deficiency in Panx3 had spontaneous systemic hypertension without obvious changes in channel function, as assessed by Ca2+ handling, ATP amounts, or Golgi luminal pH. Panx3 bound to Bcl6, and its absence reduced Bcl6 protein abundance, suggesting that the interaction with Panx3 stabilized Bcl6 by preventing its degradation. Panx3 deficiency was associated with increased expression of the gene encoding the H2O2-producing enzyme Nox4, which is normally repressed by Bcl6, resulting in H2O2-induced oxidative damage in the vasculature. Catalase rescued impaired vasodilation in mice lacking endothelial Panx3. Administration of a newly developed peptide to inhibit the Panx3-Bcl6 interaction recapitulated the increase in Nox4 expression and in blood pressure seen in mice with endothelial Panx3 deficiency. Panx3-Bcl6-Nox4 dysregulation occurred in obesity-related hypertension, but not when hypertension was induced in the absence of obesity. Our findings provide insight into a channel-independent role of Panx3 wherein its interaction with Bcl6 determines vascular oxidative state, particularly under the adverse conditions of obesity.

Correction to “Obesity-related hypertension and chronic kidney disease: from evaluation to management”

Correction to “Obesity-related hypertension and chronic kidney disease: from evaluation to management”

Cytokine and microbiota profiles in obesity-related hypertension patients.

Systemic arterial hypertension is linked to a heightened risk of cardiovascular diseases on a global scale. In Mexico, nearly half of adults in vulnerable conditions experience hypertension. Imbalance in the oral and intestinal microbiota composition has been observed in patients with hypertension, documented by a decrease of bacteria producing short-chain fatty acids, which play a critical role in blood pressure regulation. To examine the cytokines' profile and assess the characteristics of oral and gut microbiota in obesity-related hypertension in Mexican patients. A cross-sectional, observational, and analytical study was carried out. Twenty-two patients were categorized by their body mass index (BMI) as overweight and obese, and the diagnosis of primary hypertension. DNA from supragingival dental plaque and feces samples was used to carry out 16S rRNA sequencing. Additionally, 13 cytokines were quantified. In the oral microbiota, Kluyvera was found to be significantly enriched in obese compared to overweight patients. Instead, the gut microbiota was dominated by Firmicutes. However, the correlation between certain genera and proinflammatory cytokines was noted. This exploratory study provides insights into the complex relationship between the oral and gut microbiota and their association with systemic inflammation in obesity-related hypertension.

Prevention of high-fat-diet-induced obesity in mice by soluble dietary fiber from fermented and unfermented millet bran

Obesity-related diabetes, cardiovascular disease, and hypertension pose many risks to human health. Thus, mice on a high-fat diet were gavaged with millet bran (unfermented/fermented) soluble dietary fiber (RSDF/FSDF, 500 mg·kg−1) for 10 weeks in current research, and then evaluated the various biological indicators. These findings revealed that RSDF and FSDF supplements could prevent fat synthesis by inhibiting sterol regulatory element-binding protein-1c gene expression. The RSDF supplements can also accelerate fat catabolism through enhanced the mRNA expression levels of adipose triglyceride lipase and peroxisome proliferator-activated receptor α. FSDF supplements can prevent obesity by decreasing 3-hydroxy-3-methyl-glutaryl-CoA reductase expression and increasing cholesterol 7α-hydroxylase expression. Moreover, FSDF also controls obesity development by lowering total cholesterol and low-density lipoprotein cholesterol levels in the blood, triglyceride, total cholesterol, and bile acid levels in the liver. Notably, FSDF supplements can promote Bacteroides and Prevotella propagation; excretive propionic acid binds to free fatty acid receptor 2/3 and then stimulates intestinal epithelial cells to generate glucagon-like-peptide-1 and peptide YY, which can reduce food and energy intake and ultimately prevent obesity. All evidence suggests that FSDF supplements play a crucial role in preventing obesity.

The ongoing impact of obesity on childhood hypertension.

Obesity rates among children have been steadily rising over the past several decades. This epidemic has been accompanied by an increase in the prevalence of childhood hypertension, with children in low- and middle-income countries being affected to the same extent as children in high-income countries. This review will examine the trends in childhood blood pressure and the relationship between excess body weight and the development of hypertension. In addition, distinct mechanisms of obesity-related hypertension will be discussed. There will be an emphasis on recent studies conducted since the publication of new guidelines by the American Academy of Pediatrics in 2017 which resulted in the adoption of lower normative blood pressure cutoffs. The overall intent of this review is to provide the reader with an understanding of the ongoing impact, and complexities, of obesity-related hypertension.

Correlation between obesity-related indices and hypertension.

To explore the correlation between obesity-related indices and hypertension, as well as their predictive ability for hypertension, to provide new insights for the prevention and treatment of the disease. This retrospective study included participants aged over 18 years from Chongqing General Hospital, spanning January 2023 to January 2024. Based on the presence or absence of hypertension, 160 participants were divided into two groups: an observation group (with hypertension, n=83) and a control group (without hypertension, n=77). Demographic and obesity-related indices were collected to assess their correlation with hypertension. The mean waist circumference (WC) was significantly higher in the observation group 82.46 (78.87-84.35) compared to the control group 82.64 (78.00-84.87), albeit with a typographical error in reporting (P=0.012). The mean A Body Shape Index (ABSI) was significantly higher in the observation group 0.778 (0.078-0.081) compared to the control group 0.076 (0.083-0.087) (P=0.004). The mean body roundness index (BRI) was also significantly higher in the observation group 3.38 (3.07-3.84) than in the control group 3.40 (2.98-3.87) (P=0.02). Logistic regression revealed ABSI (OR=1.15, 95% CI 1.06-1.28, P=0.014), BRI (OR=1.14, 95% CI 1.03-1.23, P=0.048), and WC/BRI (OR=1.13, 95% CI 1.04-1.34, P=0.031) as statistically significant risk factors. The area under the curve values for ABSI, BRI, WC/BRI, and their combination were 0.572, 0.629, 0.652, and 0.731, respectively. ABSI, BRI, and WC/BRI may serve as independent risk factors for hypertension. These indices, individually or combined, could aid in predicting the risk of hypertension.

A case-control regression analysis of liver enzymes in obesity-induced metabolic disorders in South Asian females.

Excessive body weight may disrupt hepatic enzymes that may be aggravated by obesity-related comorbidities. The current case-control study was designed to evaluate the extent of liver enzyme alteration in obesity-related metabolic disorders. Obese females with BMI ≥ 30 suffering from metabolic disorders were grouped according to existing co-morbidity and their hepatic enzymes were compared with non-obese healthy females. The resultant data was subjected to analysis of variance and mean difference in liver enzymes were calculated at P = 0.05. Analysis of variance indicated that obese diabetic and obese hypertensive females had almost 96% and 67% increase in the concentration of gamma-glutamyl transferase than control, respectively (P<0.0001). The obese females suffering from diabetes and hypertension exhibited nearly 54% enhancement in alanine transaminase level (P<0.0001) and a 17% increase in aspartate aminotransferase concentration (P = 0.0028). Obesity along with infertility decline liver enzyme production and a 31% significant decline in aspartate aminotransferase was observed while other enzyme concentrations were not significantly altered. Regression analysis was performed on the resultant data to understand the association between liver enzyme alteration and the development of metabolic diseases. Regression analysis indicated that obese diabetic and obese diabetic hypertensive women had 20% production of normal liver enzymes and 80% enzymes produced abnormally. Obese hypertensive and obese infertile females had only 5% and 6% normal production of liver enzymes, respectively. This research leads to the conclusion that the ability of the liver to function normally is reduced in obesity-related diabetes and hypertension. This may be due to inflamed and injured liver and poses a serious threat to developing fatty liver disease and ultimately liver cirrhosis.