Role of Omega-3 Fatty Acids in Improving Metabolic Dysfunctions in Polycystic Ovary Syndrome.

Polycystic ovary syndrome (PCOS) is a common endocrine disorder that impacts women of reproductive age. In addition to reproductive and psychological complications, women with PCOS are also at a higher risk of developing metabolic diseases such as obesity, type 2 diabetes and cardiovascular disease. While weight reduction can help manage these complications in overweight or obese women, many weight loss interventions have been ineffective due to weight stigma and its psychological impact on women with PCOS. Therefore, exploring alternative dietary strategies which do not focus on weight loss per se is of importance. In this regard, omega-3 polyunsaturated fatty acids of marine origin (n-3 PUFAs), which are known for their hypotriglyceridemic, cardioprotective and anti-inflammatory effects, have emerged as a potential therapy for prevention and reversal of metabolic complications in PCOS. Several clinical trials showed that n-3 PUFAs can improve components of metabolic syndrome in women with PCOS. In this review, we first summarize the available clinical evidence for different dietary patterns in improving PCOS complications. Next, we summarize the clinical evidence for n-3 PUFAs for alleviating metabolic complications in PCOS. Finally, we explore the mechanisms by which n-3 PUFAs improve the metabolic disorders in PCOS in depth.

Beyond blood pressure, fluid and electrolyte homeostasis - Role of the renin angiotensin aldosterone system in the interplay between metabolic diseases and breast cancer.

The classical renin angiotensin aldosterone system (RAAS), as well as the recently described counter-regulatory or non-canonical RAAS have been well characterized for their role in cardiovascular homeostasis. Moreover, extensive research has been conducted over the past decades on both paracrine and the endocrine roles of local RAAS in various metabolic regulations and in chronic diseases. Clinical evidence from patients on RAAS blockers as well as pre-clinical studies using rodent models of genetic manipulations of RAAS genes documented that this system may play important roles in the interplay between metabolic diseases and cancer, namely breast cancer. Some of these studies suggest potential therapeutic applications and repurposing of RAAS inhibitors for these diseases. In this review, we discuss the mechanisms by which RAAS is involved in the pathogenesis of metabolic diseases such as obesity and type-2 diabetes as well as the role of this system in the initiation, expansion and/or progression of breast cancer, especially in the context of metabolic diseases.

Perceptions of the importance of sports nutrition knowledge and barriers in implementing them: a qualitative study among track and field stakeholders in Sri Lanka.

BACKGROUND: Integrating the core aspects of sports nutrition knowledge [SNK] into the multidisciplinary team is critical to improving an athlete's performance and well-being. Conducting in-depth interviews with members of the sports-related team is a comprehensive method of gathering information on various aspects of SNK. This qualitative study aimed to examine the opinions and beliefs of stakeholders in athletics regarding the importance of SNK. METHODS: Fifteen professional track and field athletes and stakeholders were recruited into the study. Separate in-depth interviews were conducted to collect information within four key themes. Practical difficulties in getting an appropriate meal were included in an additional theme. Thematic analysis was performed using NVIVO v10.0. RESULTS: All participants were mindful of the importance of proper food habits for overall athletic outcomes and reported different opinions on meal timing and composition. The opinions on supplements were heterogeneous and both positive and negative claims were reported. Beliefs regarding hydration demonstrated that the cohort was well aware of the significance of adequate hydration plus the signs and consequences of dehydration with many reporting experiences of the negative consequences of dehydration. All respondents reported that both alcohol and smoking may have an adverse impact on performance and health. CONCLUSIONS: All respondents emphasized the importance of proper food habits for sports performance and well-being, but also identified barriers to optimizing nutrition.

Sports Nutrition Knowledge Questionnaires Developed for the Athletic Population: a Systematic Review.

PURPOSE OF REVIEW: Sports nutrition (SN) is pivotal in aiding athletes to reach peak performance, minimize sport-related injuries, enhance career longevity, and improve general health. An accurate assessment of athletes' sports nutrition knowledge (SNK) is required to design targeted nutrition education programs aimed at enhancing both nutritional knowledge and dietary practices. This review systematically evaluates studies that use questionnaires to assess the SNK of athletes engaged in athletics. RECENT FINDINGS: The literature search was conducted in PubMed®, Web of Science®, and Scopus®, and 375 potentially relevant articles were identified. The total number of articles included in the present review is 11, with eight studies involving only athletic disciplines and three involving athletics and other sports. The majority (n = 8) of the questionnaires included general and SN aspects, with SN covering endurance athletes' knowledge of competition carbohydrate guidelines, gastrointestinal symptoms associated with exercise, and ultra-endurance athletes' sodium beliefs and practices. Questionnaires were either delivered online (n = 7) or self-administered in hard copy (n = 1). The three major strategies identified for developing questionnaires were based on previous literature and recent SN guidelines (n = 6), consultation with a panel of experts (n = 7), and the use of a previously developed sports nutrition knowledge questionnaires (SNKQ) (n = 4), with more than one approach used in five studies. Similarly, up to three validation approaches were used, including content, face, and construct validity. Seven studies used a test-retest procedure to ensure external reliability, and eight used Cronbach's alpha or kappa coefficient to assess internal consistency. Endurance and ultra-endurance athletes are the populations of interest for the majority of questionnaires developed for athletics, with most questionnaires incorporating general and SNK topics.

Temperature-Dependent Effects of Eicosapentaenoic Acid (EPA) on Browning of Subcutaneous Adipose Tissue in UCP1 Knockout Male Mice.

Uncoupling protein 1 (UCP1) plays a central role in thermogenic tissues by uncoupling cellular respiration to dissipate energy. Beige adipocytes, an inducible form of thermogenic cells in subcutaneous adipose tissue (SAT), have become a major focus in obesity research. We have previously shown that eicosapentaenoic acid (EPA) ameliorated high-fat diet (HFD)-induced obesity by activating brown fat in C57BL/6J (B6) mice at thermoneutrality (30 °C), independently of UCP1. Here, we investigated whether ambient temperature (22 °C) impacts EPA effects on SAT browning in wild-type (WT) and UCP1 knockout (KO) male mice and dissected underlying mechanisms using a cell model. We observed resistance to diet-induced obesity in UCP1 KO mice fed HFD at ambient temperature, with significantly higher expression of UCP1-independent thermogenic markers, compared to WT mice. These markers included the fibroblast growth factor 21 (FGF21) and sarco/endoplasmic reticulum Ca2+-ATPase 2b (SERCA2b), suggesting the indispensable role of temperature in beige fat reprogramming. Surprisingly, although EPA induced thermogenic effects in SAT-derived adipocytes harvested from both KO and WT mice, EPA only increased thermogenic gene and protein expression in the SAT of UCP1 KO mice housed at ambient temperature. Collectively, our findings indicate that the thermogenic effects of EPA, which are independent of UCP1, occur in a temperature-dependent manner.

Eicosapentaenoic Acid Protects against Metabolic Impairments in the APPswe/PS1dE9 Alzheimer's Disease Mouse Model.

BACKGROUND: Alzheimer's disease (AD) is an age-related neurodegenerative disease characterized by amyloid-ß (Aß) plaques. Systemic inflammation and obesity may exacerbate AD pathogenesis. We previously reported anti-inflammatory and anti-obesity effects of EPA in mice. OBJECTIVES: We aimed to determine whether EPA reduces obesity-associated metabolic dysfunctions and Aß accumulation in AD amyloidogenic mice. METHODS: Two-mo-old APPswe/PS1dE9 transgenic (TG) mice and non-TG littermates were randomly assigned to low fat (LF; 10% kcal fat), high fat (HF; 45% kcal fat), or EPA (36 g/kg)-supplemented HF diets. Body composition, glucose tolerance, and energy expenditure were measured, and serum and brain metabolic markers were tested 38 wk postintervention. Outcomes were statistically analyzed via 3-factor ANOVA, modeling genotype, sex, and diet interactions. RESULTS: HF-fed males gained more weight than females (Δ = 61 mg; P < 0.001). Compared with LF, HF increased body weights of wild-type (WT) males (Δ = 31 mg; P < 0.001). EPA reduced HF-induced weight gain in WT males (Δ = 24 mg; P = 0.054) but not in females. HF mice showed decreased glucose clearance and respiratory energy compared with LF-fed groups (Δ = -1.31 g/dL; P < 0.001), with no significant effects of EPA. However, EPA conferred metabolic improvements by decreasing serum leptin and insulin (Δ = -2.51 g/mL and Δ = -0.694 ng/mL, respectively compared with HF, P ≤ 0.05) and increasing adiponectin (Δ = 21.6 ng/mL; P < 0.001). As we expected, TG mice expressed higher serum and brain Aß than WT mice (Δ = 0.131 ng/mL; P < 0.001 and Δ = 0.56%; P < 0.01, respectively), and EPA reduced serum Aß1-40 in TG males compared with HF (Δ = 0.053 ng/mL; P ≤ 0.05). CONCLUSIONS: To our knowledge, this is the first report that EPA reduces serum Aß1-40 in obese AD male mice, warranting further investigations into tissue-specific mechanisms of EPA in AD.

Anti-inflammatory mechanisms of polyphenols in adipose tissue: role of gut microbiota, intestinal barrier integrity and zinc homeostasis.

Obesity is associated with an imbalance of micro-and macro-nutrients, gut dysbiosis, and a "leaky" gut phenomenon. Polyphenols, such as curcumin, resveratrol, and anthocyanins may alleviate the systemic effects of obesity, potentially by improving gut microbiota, intestinal barrier integrity (IBI), and zinc homeostasis. The essential micronutrient zinc plays a crucial role in the regulation of enzymatic processes, including inflammation, maintenance of the microbial ecology, and intestinal barrier integrity. In this review, we focus on IBI- which prevents intestinal lipopolysaccharide (LPS) leakage - as a critical player in polyphenol-mediated protective effects against obesity-associated white adipose tissue (WAT) inflammation. This occurs through mechanisms that block the movement of the bacterial endotoxin LPS across the gut barrier. Available research suggests that polyphenols reduce WAT and systemic inflammation via crosstalk with inflammatory NF-κB, the mammalian target of rapamycin (mTOR) signaling and zinc homeostasis.

Anti-Inflammatory Mechanisms of Curcumin and Its Metabolites in White Adipose Tissue and Cultured Adipocytes.

The plant-derived polyphenol curcumin alleviates the inflammatory and metabolic effects of obesity, in part, by reducing adipose tissue inflammation. We hypothesized that the benefits of curcumin supplementation on diet-induced obesity and systemic inflammation in mice occur through downregulation of white adipose tissue (WAT) inflammation. The hypothesis was tested in adipose tissue from high-fat diet-induced obese mice supplemented with or without curcumin and in 3T3-L1 adipocytes treated with or without curcumin. Male B6 mice were fed a high-fat diet (HFD, 45% kcal fat) with or without 0.4% (w/w) curcumin supplementation (HFC). Metabolic changes in these mice have been previously reported. Here, we determined the serum levels of the curcumin metabolites tetrahydrocurcumin (THC) and curcumin-O-glucuronide (COG) using mass spectrometry. Moreover, we determined interleukin 6 (IL-6) levels and proteomic changes in LPS-stimulated 3T3-L1 adipocytes treated with or without curcumin by using immunoassays and mass spectrometry, respectively, to gain further insight into any altered processes. We detected both curcumin metabolites, THC and COG, in serum samples from the curcumin-fed mice. Both curcumin and its metabolites reduced LPS-induced adipocyte IL-6 secretion and mRNA levels. Proteomic analyses indicated that curcumin upregulated EIF2 and mTOR signaling pathways. Overall, curcumin exerted anti-inflammatory effects in adipocytes, in part by reducing IL-6, and these effects may be linked to the upregulation of the mTOR signaling pathway, warranting additional mechanistic studies on the effects of curcumin and its metabolites on metabolic health.

Effects of captopril on glucose metabolism and autophagy in liver and muscle from mice with type 1 diabetes and diet-induced obesity.

Impaired metabolic functions underlie the pathophysiology of diabetes and obesity. The renin-angiotensin system (RAS) is one pathway related to the pathophysiology of both diseases. RAS activation in metabolically active tissues exerts pro-inflammatory effects via angiotensin II (Ang II), linked to dysfunction in cellular processes such as autophagy, which is associated with obesity and diabetes. Here, we determined whether RAS is involved in metabolic dysregulations in a Type 1 Diabetes (T1D) mouse model, treated with captopril, and in an obesity mouse model (Agt-Tg) that overexpresses angiotensinogen (Agt) in adipose tissue. T1D mice had lower plasma leptin, resistin and higher non-esterified fatty acids (NEFA) compared to wild type (Wt) mice, even under captopril treatment. Further, mRNA levels for Agt, At1, Insr, and Beclin1 were upregulated in muscle and liver of T1D mice with captopril compared to Wt. Moreover, autophagy markers LC3 and p62 proteins were decreased, regardless of captopril treatment in the liver from T1D mice. In obese Wt mice, captopril increased muscle Irs1 gene levels. Further, captopril reduced mRNA levels of At1, Insr, Ampk, Beclin1, Atg12, and Lc3 in the liver from both Wt and Agt-Tg mice, while Agt, At1, Insr, and Atg12 expression was reduced in Agt-Tg mice without captopril treatment. Irs1 expression was decreased in the liver from obese Wt mice treated with captopril. Our results suggest that captopril treatment upregulates components of RAS, insulin signaling, and autophagy in both muscle and liver, indicating potential utility of captopril in targeting both insulin sensitivity and autophagy in diabetes and obesity.

Sex-Dependent Effects of Eicosapentaenoic Acid on Hepatic Steatosis in UCP1 Knockout Mice.

Visceral obesity may be a driving factor in nonalcoholic fatty liver disease (NAFLD) development. Previous studies have shown that the omega-3 polyunsaturated fatty acid, eicosapentaenoic acid (EPA), ameliorates obesity in high-fat (HF) fed male, C57Bl/6 mice at thermoneutral conditions, independent of uncoupling protein 1 (UCP1). Our goals herein were to investigate sex-dependent mechanisms of EPA in the livers of wild type (WT) and UCP1 knockout (KO) male and female mice fed a HF diet (45% kcal fat; WT-HF, KO-HF) with or without supplementation of 36 g/kg EPA (WT-EPA, KO-EPA). KO significantly increased body weight in males, with no significant reductions with EPA in the WT or KO groups. In females, there were no significant differences in body weight among KO groups and no effects of EPA. In males, liver TGs were significantly higher in the KO-HF group and reduced with EPA, which was not observed in females. Accordingly, gene and protein markers of mitochondrial oxidation, peroxisomal biogenesis and oxidation, as well as metabolic futile cycles were sex-dependently impacted by KO and EPA supplementation. These findings suggest a genotypic difference in response to dietary EPA supplementation on the livers of male and female mice with diet-induced obesity and housed at thermoneutrality.

Mechanisms linking endoplasmic reticulum (ER) stress and microRNAs to adipose tissue dysfunction in obesity.

Over accumulation of lipids in adipose tissue disrupts metabolic homeostasis by affecting cellular processes. Endoplasmic reticulum (ER) stress is one such process affected by obesity. Biochemical and physiological alterations in adipose tissue due to obesity interfere with adipose ER functions causing ER stress. This is in line with increased irregularities in other cellular processes such as inflammation and autophagy, affecting overall metabolic integrity within adipocytes. Additionally, microRNAs (miRNAs), which can post-transcriptionally regulate genes, are differentially modulated in obesity. A better understanding and identification of such miRNAs could be used as novel therapeutic targets to fight against diseases. In this review, we discuss ways in which ER stress participates as a common molecular process in the pathogenesis of obesity-associated metabolic disorders. Moreover, our review discusses detailed underlying mechanisms through which ER stress and miRNAs contribute to metabolic alteration in adipose tissue in obesity. Hence, identifying mechanistic involvement of miRNAs-ER stress cross-talk in regulating adipose function during obesity could be used as a potential therapeutic approach to combat chronic diseases, including obesity.

Eicosapentaenoic Acid Regulates Inflammatory Pathways through Modulation of Transcripts and miRNA in Adipose Tissue of Obese Mice.

This study aims to investigate the global profiling of genes and miRNAs expression to explore the regulatory effects of eicosapentaenoic acid (EPA) in visceral adipose tissue (VAT) of obese mice. We used male mice, fed either a high-fat diet (HF) or HF supplemented with EPA (HF-EPA), for 11 weeks. RNA, and small RNA profiling, were performed by RNAseq analysis. We conducted analyses using Ingenuity Pathway Analysis software (IPA®) and validated candidate genes and miRNAs related to lipid mediators and inflammatory pathways using qRT-PCR. We identified 153 genes differentially downregulated, and 62 microRNAs differentially expressed in VAT from HF-EPA compared to HF. Genes with a positive association with inflammation, chemotaxis, insulin resistance, and inflammatory cell death, such as Irf5, Alox5ap, Tlrs, Cd84, Ccr5, Ccl9, and Casp1, were downregulated by EPA. Moreover, EPA significantly reduced LTB4 levels, a lipid mediator with a central role in inflammation and insulin resistance in obesity. The pathways and mRNA/microRNA interactions identified in our study corroborated with data validated for inflammatory genes and miRNAs. Together, our results identified key VAT inflammatory targets and pathways, which are regulated by EPA. These targets merit further investigation to better understand the protective mechanisms of EPA in obesity-associated inflammation.

Effectiveness of Low-dose Ethinylestradiol/Cyproterone Acetate and Ethinylestradiol/Desogestrel with and without Metformin on Hirsutism in Polycystic Ovary Syndrome: A Randomized, Double-blind, Triple-dummy Study.

BACKGROUND: The effectiveness of different combined oral contraceptive pills and metformin in reducing hirsutism in patients with polycystic ovary syndrome (PCOS) remains unclear. OBJECTIVE: We sought to determine the effects of ethinylestradiol (35µg)/cyproterone acetate (2mg) (EE/CPA) and ethinylestradiol (20µg)/desogestrel (0.15mg) (EE/DES), alone or with metformin, on hirsutism in PCOS. METHODS: A randomized, double-blind, triple-dummy study was conducted on women with PCOS and hirsutism (N=107) who received one of four drug combinations (Arm A: EE/CPA; Arm B: EE/DES; Arm C: EE/CPA plus metformin; or Arm D: EE/DES plus metformin). Hirsutism was assessed at baseline, six months, and 12 months by using five outcomes variables. RESULTS: No outcomes variable showed a significant difference between the four arms at 12 months. There was a significant reduction in both hair density and modified Ferriman-Gallwey score (mFGS) in Arm A, mFGS in Arm B, hair density in Arm C, and diameter of sideburn hair in Arm D, respectively. Separately, there was a significant increase noted in the hair growth rate of chin and an improvement in patients' perceptions of hirsutism in all four study arms. CONCLUSION: EE/CPA and EE/DES were equally effective in improving hirsutism in PCOS, with no added benefit from low-dose metformin. Sri Lanka Clinical Trials Registry (http://www.slctr.lk) registration no. SLCTR/2015/007.

AdipoGauge software for analysis of biological microscopic images.

Obesity is a complex disease of global epidemic proportions. Adipose tissue expansion and chronic low-grade inflammation, locally and systemically, are hallmark features of obesity. Obesity is associated with several other chronic diseases, which are also characterized by inflammation. Determination of adipocyte size and macrophage content in adipose tissue is a critical step in assessing changes in this tissue with obesity. Here, we introduce a complete standalone software package, AdipoGauge, to analyse microscopic images derived from haematoxylin and eosin (H&E)-stained and immunofluorescently stained histology sections of adipose tissue. The software package is a user-friendly application that does not require a vast knowledge of computer science or costly commercial tools. AdipoGauge includes analysing tools that are capable of cell counting and colour separation. Furthermore, it can quantify the cell data in images both with and without clear boundaries around the cells. It can also remove objects from the image that are not intended for analysis, such as blood vessels or partial cells at edges of slide sections. The simple and state-of-the-art graphical user interface requires minimal time and learning.

Omega-3 Fatty Acids and Adipose Tissue: Inflammation and Browning.

White adipose tissue (WAT) and brown adipose tissue (BAT) are involved in whole-body energy homeostasis and metabolic regulation. Changes to mass and function of these tissues impact glucose homeostasis and whole-body energy balance during development of obesity, weight loss, and subsequent weight regain. Omega-3 polyunsaturated fatty acids (ω-3 PUFAs), which have known hypotriglyceridemic and cardioprotective effects, can also impact WAT and BAT function. In rodent models, these fatty acids alleviate obesity-associated WAT inflammation, improve energy metabolism, and increase thermogenic markers in BAT. Emerging evidence suggests that ω-3 PUFAs can also modulate gut microbiota impacting WAT function and adiposity. This review discusses molecular mechanisms, implications of these findings, translation to humans, and future work, especially with reference to the potential of these fatty acids in weight loss maintenance.

Role of microRNA 690 in Mediating Angiotensin II Effects on Inflammation and Endoplasmic Reticulum Stress.

Overactivation of the renin-angiotensin system (RAS) during obesity disrupts adipocyte metabolic homeostasis and induces endoplasmic reticulum (ER) stress and inflammation; however, underlying mechanisms are not well known. We propose that overexpression of angiotensinogen (Agt), the precursor protein of RAS in adipose tissue or treatment of adipocytes with Angiotensin II (Ang II), RAS bioactive hormone, alters specific microRNAs (miRNA), that target ER stress and inflammation leading to adipocyte dysfunction. Epididymal white adipose tissue (WAT) from B6 wild type (Wt) and transgenic male mice overexpressing Agt (Agt-Tg) in adipose tissue and adipocytes treated with Ang II were used. Small RNA sequencing and microarray in WAT identified differentially expressed miRNAs and genes, out of which miR-690 and mitogen-activated protein kinase kinase 3 (MAP2K3) were validated as significantly up- and down-regulated, respectively, in Agt-Tg, and in Ang II-treated adipocytes compared to respective controls. Additionally, the direct regulatory role of miR-690 on MAP2K3 was confirmed using mimic, inhibitors and dual-luciferase reporter assay. Downstream protein targets of MAP2K3 which include p38, NF-κB, IL-6 and CHOP were all reduced. These results indicate a critical post-transcriptional role for miR-690 in inflammation and ER stress. In conclusion, miR-690 plays a protective function and could be a useful target to reduce obesity.

Nutrients and Immunometabolism: Role of Macrophage NLRP3.

Inflammation is largely mediated by immune cells responding to invading pathogens, whereas metabolism is oriented toward producing usable energy for vital cell functions. Immunometabolic alterations are considered key determinants of chronic inflammation, which leads to the development of chronic diseases. Studies have demonstrated that macrophages and the NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasome are activated in key metabolic tissues to contribute to increased risk for type 2 diabetes mellitus, Alzheimer disease, and liver diseases. Thus, understanding the tissue-/cell-type-specific regulation of the NLRP3 inflammasome is crucial for developing intervention strategies. Currently, most of the nutrients and bioactive compounds tested to determine their inflammation-reducing effects are limited to animal models. Future studies need to address how dietary compounds regulate immune and metabolic cell reprograming in humans.

Autophagy in metabolic syndrome: breaking the wheel by targeting the renin-angiotensin system.

Metabolic syndrome (MetS) is a complex, emerging epidemic which disrupts the metabolic homeostasis of several organs, including liver, heart, pancreas, and adipose tissue. While studies have been conducted in these research areas, the pathogenesis and mechanisms of MetS remain debatable. Lines of evidence show that physiological systems, such as the renin-angiotensin system (RAS) and autophagy play vital regulatory roles in MetS. RAS is a pivotal system known for controlling blood pressure and fluid balance, whereas autophagy is involved in the degradation and recycling of cellular components, including proteins. Although RAS is activated in MetS, the interrelationship between RAS and autophagy varies in glucose homeostatic organs and their cross talk is poorly understood. Interestingly, autophagy is attenuated in the liver during MetS, whereas autophagic activity is induced in adipose tissue during MetS, indicating tissue-specific discordant roles. We discuss in vivo and in vitro studies conducted in metabolic tissues and dissect their tissue-specific effects. Moreover, our review will focus on the molecular mechanisms by which autophagy orchestrates MetS and the ways future treatments could target RAS in order to achieve metabolic homeostasis.

Undiagnosed diabetes, hypertension, and hypercholesterolaemia in an overweight or obese population: implications for cardiovascular disease risk screening programme.

INTRODUCTION: Establishing the burden of undiagnosed CVD risk factors is critical to monitoring public health efforts related to screening and diagnosis. OBJECTIVE: To assess the proportion and determinants of undiagnosed diabetes, hypertension, and hypercholesterolaemia, among overweight or obese adults. METHODS: A sample of 1200 participants aged 35-64 years with a BMI ≥25 kg/m2 was selected from the Colombo district. Data were collected through a questionnaire, anthropometry, blood pressure measurement, and blood sampling for fasting plasma glucose, HbA1c, and lipid profile. Undiagnosed diabetes, hypertension, and hypercholesterolaemia were defined as fasting plasma glucose ≥126 mg/dL or HbA1c ≥6.5%; systolic blood pressure ≥140 mmHg or diastolic blood pressure ≥90 mmHg; total cholesterol ≥240 mg/dl respectively, in a person without a previous diagnosis. Multiple logistic regression analyses were carried out to identify determinants. RESULTS: The prevalence (95%CI) of diabetes was 28% (25.5, 30.5), hypertension, 33.4% (30.7, 36.1) and hypercholesterolaemia, 31.9% (29.2, 34.5). The proportion of undiagnosed diabetes was 13.8% (11.9, 15.8), undiagnosed hypertension 11.3% (9.5, 13.1), and undiagnosed hypercholesterolaemia 17.8% (15.6, 19.9). Undiagnosed cases accounted for almost half of all diabetes cases, one-third of all hypertension cases, and more than half (56%) of all high cholesterol cases. The key determinants for undiagnosed CVD risk were: male sex, low or middle income, rural residence, and relatively younger age. CONCLUSION: CVD screening programmes should be tailored to target populations based on these determinants and provide basic diagnostic facilities in all health centres. The 'proportion undiagnosed' in the population may be a useful indicator to evaluate their effectiveness.

High Prevalence of Overweight/Obesity in Urban Sri Lanka: Findings from the Colombo Urban Study.

BACKGROUND: South Asian countries face a double burden of malnutrition characterized by high prevalence of underweight, overweight, and obesity. Understanding the distribution of this public health problem is important to tailor targeted interventions for communities. The objective of the current study was to find out the prevalence of obesity in urban Sri Lanka and to identify sociodemographic factors associated with it. METHODS: Adult males and females residing in an urban government division of the Colombo District in Sri Lanka were included in this study (Colombo Urban Study). Stratified simple random sampling was used to select a sample of 463 from the total population. Sociodemographic data using an interviewer-administered questionnaire, anthropometric measurements, and serum samples were obtained for investigations. RESULTS: When the global BMI cutoffs were applied, the community prevalences of underweight, normal weight, overweight, and obesity were 7.7%, 39.6%, 37.0%, and 15.8%, respectively. When the Asian BMI cutoffs were applied, the respective prevalences were 7.7%, 26.8%, 34.3%, and 31.2%. The community prevalence for abdominal obesity was 58.1% when using Asian cutoffs. Females had a higher prevalence of both obesity and abdominal obesity. There was an ethnic difference in obesity rates with Moors having the highest rates (65.5%) followed by Sinhalese (52.3%) and Tamils (40.2%). The highest obesity prevalence was observed in the most educated group. Multiple regression analysis showed that high BMI was associated with female gender and family history of hypertension. Serum LDL negatively associated with BMI while the strength of this relationship was impacted by serum HBA1c levels. Finally, serum triglyceride level showed positive association with BMI, and the effect was more marked in Moors compared to Sinhalese. CONCLUSION: Two-thirds of adults in the studied urban population were overweight or obese. This highlights the urgent need for interventions to curb this epidemic. The gender, ethnic differences in obesity, its associations with educational status, and the interactions with metabolic comorbidities indicate that these interventions may need to be targeted towards different groups in the population.