Related Cardiometabolic Diseases Research Articles

Longitudinal serum proteome mapping reveals biomarkers for healthy ageing and related cardiometabolic diseases.

The blood proteome contains biomarkers of ageing and age-associated diseases, but such markers are rarely validated longitudinally. Here we map the longitudinal proteome in 7,565 serum samples from a cohort of 3,796 middle-aged and elderly adults across three time points over a 9-year follow-up period. We pinpoint 86 ageing-related proteins that exhibit signatures associated with 32 clinical traits and the incidence of 14 major ageing-related chronic diseases. Leveraging a machine-learning model, we pick 22 of these proteins to generate a proteomic healthy ageing score (PHAS), capable of predicting the incidence of cardiometabolic diseases. We further identify the gut microbiota as a modifiable factor influencing the PHAS. Our data constitute a valuable resource and offer useful insights into the roles of serum proteins in ageing and age-associated cardiometabolic diseases, providing potential targets for intervention with therapeutics to promote healthy ageing.

Effects of Cynara scolymus L. Bract Extract on Lipid Metabolism Disorders Through Modulation of HMG-CoA Reductase, Apo A-1, PCSK-9, p-AMPK, SREBP-2, and CYP2E1 Expression.

Background/Objectives: Hyperlipidemia is a major contributor to metabolic complications and tissue damage, leading to conditions such as liver steatosis, atherosclerosis, and obesity. This study aimed to investigate the effects of aqueous artichoke bract extract (AE) on lipid metabolism, liver antioxidative defense, and liver steatosis in mice fed a high-fat, high-sucrose diet while elucidating the underlying mechanisms. Methods: An 8-week study used hyperlipidemic mice treated with AE at daily doses of 100 and 200 mg/kg bw, compared to fenofibrate. Plasma, liver, fecal, and biliary lipids, as well as blood glucose, were analyzed enzymatically. The liver antioxidative defense was assessed by measuring reduced glutathione, malondialdehyde (MDA), and antioxidant enzyme activities, while liver steatosis was evaluated through transaminase and alkaline phosphatase activities and histological monitoring of lipid droplets. Polyphenol profiling and quantification were performed using HPLC-DAD, and potential mechanisms were predicted by molecular docking and confirmed in HepG2 cells. Results: At 200 mg/kg, AE significantly improved plasma lipid profiles by reducing total cholesterol, triglycerides, and LDL-cholesterol while increasing HDL-cholesterol. It facilitated cholesterol reduction in the liver and its excretion, indicating activation of reverse cholesterol transport, which led to reduced body weight and liver steatosis. AE lowered MDA levels and enhanced antioxidant enzyme activities. AE was found to be safe (LD50 > 5000 mg/kg) and modulated gene expression in HepG2 cells. Conclusions: Based on our results, the artichoke bract extract could be considered a natural resource of bioactive compounds to treat hyperlipidemia and related cardiometabolic diseases.

Abstract 14690: ProduceRX Clinical Trial

Background: Nutrition related cardiometabolic diseases are leading causes of morbidity, health disparities and health care spending. Produce prescriptions are highly promising to address these issues but impacts on health outcomes have not been tested in a randomized controlled trial. Hypothesis: A pre-randomized controlled trial that provides 6 months of free weekly produce deliveries to the intervention group reduces hemoglobin A1c (HbA1c), body mass index (BMI), and blood pressure (BP), among Medicaid patients with type 2 diabetes (T2DM) and persistently elevated HbA1c when compared to the control group. Methods: A total of 450 eligible Kaiser Permanente Southern California patients were enrolled 1:1:1 into control, high- and low-dose intervention groups. Eligibility criteria included: being enrolled through Medicaid (MediCal), age 18+ years, having T2DM with at least two HbA1c values > 7.5% in the past 12 months. Produce amounts were scaled to household size and ranged from $90-270 and $90-180 for high and low-dose households, respectively. The primary endpoint was change in HbA1c at 6 months (measured up to 90 days post-intervention). Secondary outcomes were changes in BMI and BP. Primary analysis assessed both intervention groups compared to control; exploratory analyses considered dose-response. Analysis was conducted using random effects models. Results: Participants were predominantly Hispanic (85%), female (65%), and in average 59.4(SD=13.2) years old. At baseline, HbA1c was 9.40% (1.52); BMI 34.1kg/m2 (7.95); 74% had elevated BP or hypertension (stage 1 or 2), 58.3% were food insecure. Baseline characteristics were similar between control and intervention groups, 87% of participants had a 6-month HbA1c measure. In intention-to-treat analysis, compared to control, HbA1c at 6 months was significantly reduced in the intervention group: -0.37 [95%CI:-0.71;-0.04],p=0.028. Reduction in HbA1c was not significantly different between the high- and low-dose intervention. Results for BMI and BP are forthcoming. Conclusion: In the first randomized controlled trial of its kind, a produce prescription program significantly improved HbA1c among low-income patients on Medicaid with poor glycemic control at baseline.

Gender differences in the risk of developing obesity related disease can be explained by sex‐specific molecular signatures that regulates adipose endothelial cell growth

Obesity is the excessive growth of adipose tissue resulting from the chronic consumption of excess calories and is a recognised risk factor for developing cardio-metabolic diseases. There is however a significant variation in the size and expandibility of different adipose tissue in humans. The inability of adipose tissue to expand “safely” leads to ectopic fat deposition, causing insulin resistance, type 2 diabetes and cardiovascular conditions – which are more prevalent in men than women. Thus, the mechanisms that control the expandability of adipose tissue are key factors in determining diabetes risk in obesity. An interesting study from York University have provided new insights on the biological underpinning in gender differences in the risk of developing obesity-related diseases. Previous study from this group has observed that when mice become obese, females grow more new blood vessels to supply the expanding fat tissue with oxygen and nutrients, whereas males grow a lot less. To understand the mechanism regulating this, the team used software to help sift through thousands of genes to zero in on the ones that would be associated with blood vessel growth. They discovered that processes associated with the proliferation of new blood vessels were high in the female mice, whereas the males had a high level of processes associated with inflammation. Thereafter, the investigators examined the behaviour of the endothelial cells ex-vivo. Interestingly, they observed that even when these cells were studied ex-vivo, male and female endothelial cells still behave very differently from each other - female endothelial cells replicated faster, while male endothelial cells displayed greater sensitivity to an inflammatory stimulus. Further studies to investigate the effects of specific genes in humans that regulate endothelial cells growth will provide potential therapeutic target to manage and treat obesity related cardio-metabolic diseases. The study was funded by a grant through the Canadian Institutes of Health Research, as well as the Natural Science and Engineering Research Council of Canada and York's Faculty of Health.

Clinical traits and systemic risks of familial diabetes mellitus according to age of onset and quantity: an analysis of data from the community-based KoGES cohort study.

The aim of this study was to clarify the clinical trait of familial diabetes mellitus (DM) by analyzing participants' risk of DM according to the age of DM onset in parents and siblings, and to evaluate individuals' risk of DM-associated cardiometabolic diseases. Altogether, 211,173 participants aged ≥40 years from the Korean Genome and Epidemiology Study were included in this study. The participants were divided into groups based on the number (1 or 2 relatives) and age of onset (no DM and early, common, or late onset) of familial DM. Participants' risk of DM was assessed using a Cox regression model with hazard ratios and 95% confidence intervals (CIs). A logistic regression model with odds ratios was used to evaluate associations among the participants' likelihood of acquiring cardiometabolic diseases such as hypertension, chronic kidney disease (CKD), and cardiovascular disease. The risk of developing DM was 2.02-fold (95% CI, 1.88 to 2.18) and 2.88-fold (95% CI, 2.50 to 3.33) higher, respectively, in participants with 1 and 2 family members diagnosed with familial DM. It was 2.72-fold (95% CI, 2.03 to 3.66) higher in those with early-onset familial DM. In the early-onset group, the respective risks of hypertension and CKD were 1.87-fold (95% CI, 1.37 to 2.55) and 4.31-fold (95% CI, 2.55 to 7.27) higher than in the control group. The risk of DM and related cardiometabolic diseases was positively associated with the number of family members diagnosed with DM and an early diagnosis in family members with DM.

Asprosin Exerts Pro-Inflammatory Effects in THP-1 Macrophages Mediated via the Toll-like Receptor 4 (TLR4) Pathway.

Adipose tissue is a dynamic endocrine organ, secreting a plethora of adipokines which play a key role in regulating metabolic homeostasis and other physiological processes. An altered adipokine secretion profile from adipose tissue depots has been associated with obesity and related cardio-metabolic diseases. Asprosin is a recently described adipokine that is released in response to fasting and can elicit orexigenic and glucogenic effects. Circulating asprosin levels are elevated in a number of cardio-metabolic diseases, including obesity and type 2 diabetes. In vitro studies have reported pro-inflammatory effects of asprosin in a variety of tissues. The present study aimed to further elucidate the role of asprosin in inflammation by exploring its potential effect(s) in THP-1 macrophages. THP-1 monocytes were differentiated to macrophages by 48 h treatment with dihydroxyvitamin D3. Macrophages were treated with 100 nM recombinant human asprosin, 100 ng/mL lipopolysaccharide (LPS), and 10 μM caffeic acid phenethyl ester (CAPE; an inhibitor of NFκB activation) or 1 µM TAK-242 (a Toll-like receptor 4, TLR4, inhibitor). The expression and secretion of pertinent pro-inflammatory mediators were measured by qPCR, Western blot, ELISA and Bioplex. Asprosin stimulation significantly upregulated the expression and secretion of the pro-inflammatory cytokines: tumour necrosis factor α (TNFα), interleukin-1β (IL-1β), IL-8 and IL-12 in vitro. This pro-inflammatory response in THP-1 macrophages was partly attenuated by the treatments with CAPE and was significantly inhibited by TAK-242 treatment. Asprosin-induced inflammation is significantly counteracted by TLR4 inhibition in THP-1 macrophages, suggesting that asprosin exerts its pro-inflammatory effects, at least in part, via the TLR4 signalling pathway.

Fecal microbiota composition is related to brown adipose tissue 18F-fluorodeoxyglucose uptake in young adults

ObjectiveHuman brown adipose tissue (BAT) has gained considerable attention as a potential therapeutic target for obesity and its related cardiometabolic diseases; however, whether the gut microbiota might be an efficient stimulus to activate BAT metabolism remains to be ascertained. We aimed to investigate the association of fecal microbiota composition with BAT volume and activity and mean radiodensity in young adults.Methods82 young adults (58 women, 21.8 ± 2.2 years old) participated in this cross-sectional study. DNA was extracted from fecal samples and 16S rRNA sequencing was performed to analyse the fecal microbiota composition. BAT was determined via a static 18F-fluorodeoxyglucose (18F-FDG) positron emission tomography-computed tomography scan (PET/CT) after a 2 h personalized cooling protocol. 18F-FDG uptake was also quantified in white adipose tissue (WAT) and skeletal muscles.ResultsThe relative abundance of Akkermansia, Lachnospiraceae sp. and Ruminococcus genera was negatively correlated with BAT volume, BAT SUVmean and BAT SUVpeak (all rho ≤ − 0.232, P ≤ 0.027), whereas the relative abundance of Bifidobacterium genus was positively correlated with BAT SUVmean and BAT SUVpeak (all rho ≥ 0.262, P ≤ 0.012). On the other hand, the relative abundance of Sutterellaceae and Bifidobacteriaceae families was positively correlated with 18F-FDG uptake by WAT and skeletal muscles (all rho ≥ 0.213, P ≤ 0.042). All the analyses were adjusted for the PET/CT scan date as a proxy of seasonality.ConclusionOur results suggest that fecal microbiota composition is involved in the regulation of BAT and glucose uptake by other tissues in young adults. Further studies are needed to confirm these findings.Clinical trial informationClinicalTrials.gov no. NCT02365129 (registered 18 February 2015).

Novel insights into the pathological development of dyslipidemia in patients with hypothyroidism.

According to the previous reports, hypothyroidism has been shown to be strongly correlated with increased circulating concentrations of total cholesterol, low-density lipoprotein cholesterol, and triglycerides. Notably, thyroid hormones are confirmed to modulate the production, clearance, and transformation process of cholesterol within circulation of mammals. Moreover, emerging evidence suggests that the thyroid-stimulating hormone could also participate in modulating serum lipid metabolism independently of thyroid hormones, which further induces the pathological development of dyslipidemia. However, the underlying mechanism is still not fully elucidated. Recently, several research studies have demonstrated that the pathogenic progression of hypothyroidism-related dyslipidemia might be correlated with the decreased serum concentrations of thyroid hormones and the increased serum concentrations of thyroid-stimulating hormones. Thus, this indicates that hypothyroidism could induce dyslipidemia and its related cardio-metabolic disorder diseases. In addition, several newly identified modulatory biomarkers, such as proprotein convertase subtilisin/kexin type 9, angiopoietin-like protein, and fibroblast growth factors, might play an important role in the regulation of dyslipidemia induced by hypothyroidism. Furthermore, under the status of hypothyroidism, significantly dysfunctional HDL particles could also be observed. In the current review, we summarized the recent knowledge of the relationship between the developments of hypothyroidism with dyslipidemia. We also discussed the updated understanding of the mechanisms whereby hypothyroidism induces the risk and the development of dyslipidemia and cardio-metabolic diseases.

A patent review of aldosterone synthase inhibitors (2014-present)

ABSTRACT Introduction Aldosterone synthase (AS) is a key enzyme involved in the final three rate-limiting steps of the biosynthesis pathway of aldosterone, and its inhibition has been considered as an effective strategy to treat hypertension, heart failure, and related cardio-metabolic diseases. Area covered This review provides an update on the discovery and development of aldosterone synthase inhibitors by means of patents published between January 2014 and March 2021. The molecules are classified by pharmaceutical company with progress that has been made in clinical trials being highlighted. Expert opinion Mineralocorticoid receptor antagonists (MRAs) and aldosterone synthase inhibitors (ASI) represent two of the main approaches for the blockade of aldosterone. Clinical success, as well as foreseen side effects of steroidal MRAs, prompted the discovery and development of ASI. Since the observation of decreased cortisol levels in clinical trials for LCI699, subsequent efforts have been largely focused on improving its selectivity over hCYP11B1. Candidates with improved potency and selectivity are under investigation across a wide range of indications. Whether ASI will provide an additional therapeutic advantage over current safe and selective non-steroidal MRAs is highly anticipated.

A Growing Journey From Neurotrophins To Metabotrophins In Cardiometabolic Diseases

Currently, obesity has been recognized as a prime risk in the development of car-diometabolic diseases (CMD) and neurodegenerative diseases (NDD). The patho-genesis and therapy of CMD are immensely complex at the cellular and molecular levels. This scenario raises the question of how such a complexity may be grappled in a more tangible manner. Since 2003, we have been thinking “what nobody has yet thought about that everybody sees”, namely, matabotrophic factors (MTF, metabotrophins). The latter include mainly (i) the neurotrophins nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF), and (ii) the adipomyo-kines adiponectin, irisin, BDNF, fibroblast growth factor-21 alike as adipose- and skeletal muscle-derived signaling proteins (these latter discussed in another review in the present volume of Adipobiology). Herein, we argue that obesity and related CMD and NDD, particularly Alzheimer’s disease, may be viewed as MTF-deficient diseases. Further studies on MTF signatures and ramifications in these diseases are required. These would provide greater insights on how we can make MTF work for the improvement of physiological and psychological quality of human life.

Adipomyobiology Of Obesity And Related Diseases: Therapy Insights

Today, the most widespread disease around the world is not COVID-19 or any other communicable disease. Indeed, obesity and type 2 diabetes mellitus (T2DM) have been recognized as the main risks for cardiometabolic diseases (CMD) and their morbidity and mortality signature. Recent studies revealed that the adipose tissue and the skeletal muscles may function as endocrine and paracrine organs secreting multiple proteins termed adipokines and myokines respectively. Some of them being produced both by adipose and skeletal tissue, hence dubbed adipomyokines. The contents of this review highlights the following two topics: (i) the progress in knowledge of adipomyokines may lead to better understandings of the process of pathogenesis of obesity and related CMD, and (ii) in-depth studies on Palade-Blobel’s general theory of cell protein secretion may allow to explore its pharmacological potentials for new therapies of these diseases. This may open up an intriguing line of scientific enquiry that will unite adipobiologists and myobiologists in the fight against obesity and related CMD.

Cardio- and Neurometabolic Adipobiology: Consequences and Implications for Therapy

Studies over the past 30 years have revealed that adipose tissue is the major endocrine and paracrine organ of the human body. Arguably, adiopobiology has taken its reasonable place in studying obesity and related cardiometabolic diseases (CMDs), including Alzheimer’s disease (AD), which is viewed herein as a neurometabolic disorder. The pathogenesis and therapy of these diseases are multiplex at basic, clinical and translational levels. Our present goal is to describe new developments in cardiometabolic and neurometabolic adipobiology. Accordingly, we focus on adipose- and/or skeletal muscle-derived signaling proteins (adipsin, adiponectin, nerve growth factor, brain-derived neuroptrophic factor, neurotrophin-3, irisin, sirtuins, Klotho, neprilysin, follistatin-like protein-1, meteorin-like (metrnl), as well as growth differentiation factor 11) as examples of metabotrophic factors (MTFs) implicated in the pathogenesis and therapy of obesity and related CMDs. We argue that these pathologies are MTF-deficient diseases. In 1993 the “vascular hypothesis of AD” was published and in the present review we propose the “vasculometabolic hypothesis of AD.” We discuss how MTFs could bridge CMDs and neurodegenerative diseases, such as AD. Greater insights on how to manage the MTF network would provide benefits to the quality of human life.

Receptor-Mediated ER Export of Lipoproteins Controls Lipid Homeostasis in Mice and Humans

Efficient delivery of specific cargos invivo poses a major challenge to the secretory pathway, which shuttles products encoded by ∼30% of the genome. Newly synthesized protein and lipid cargos embark on the secretory pathway via COPII-coated vesicles, assembled by the GTPase SAR1 on the endoplasmic reticulum (ER), but how lipid-carrying lipoproteins are distinguished from the general protein cargos in the ER and selectively secreted has not been clear. Here, we show that this process is quantitatively governed by the GTPase SAR1B and SURF4, a high-efficiency cargo receptor. While both genes are implicated in lipid regulation in humans, hepatic inactivation of either mouse Sar1b or Surf4 selectively depletes plasma lipids to near-zero and protects the mice from atherosclerosis. These findings show that the pairing between SURF4 and SAR1B synergistically operates a specialized, dosage-sensitive transport program for circulating lipids, while further suggesting a potential translation to treat atherosclerosis and related cardio-metabolic diseases.

Importance of Measured Body Fat, Visceral Adiposity Index, and Lipid Accumulation Product Index in Predicting Cardiometabolic Risk Factors.

Background: Obesity, which is defined as excessive fat accumulation in the body, is an important public health problem. Objective: The aim of this study was to compare measured body fat and the visceral adiposity index (VAI) and lipid accumulation product (LAP) index used to predict cardiometabolic risk (CMR) factors. Methods: This study was performed retrospectively by scanning the files of 817 participants who had bioelectrical impedance analysis (BIA) results and routine blood tests. The VAI and the LAP index were calculated using the appropriate formulas. Results: Of the 817 participants included in the study, 67.9% (n = 555) were female, 32.1% (n = 262) were male, and the mean age was 36.14 ± 11.4 (18-65) years. The mean body mass index (BMI) was 29.90 ± 6.6 kg/m2 and 24.2% (n = 198) of the participants were of normal weight (BMI <25 kg/m2), while 75.8% (n = 619) were overweight or obese (BMI ≥25 kg/m2). Body fat quantity was higher in females than in males. As BMI increased, the body fat quantity measured by BIA also increased (P < 0.001). The mean LAP index of men was higher than the mean LAP index of women in both the normal-weight group and the obese group (P = 0.025 and P = 0.033, respectively). One unit increase in visceral fat percentage resulted in a 77.9% increase in CMR. Conclusions: It may not be sufficient to use only BMI to predict obesity and related cardiometabolic diseases. According to the study findings, it was determined that the increase in visceral fat percentage significantly increases the CMR.

Race affects the association of obesity measures with insulin sensitivity

Race differences in body composition and fat distribution may in part explain the differences in insulin sensitivity and the disproportionate burden of type 2 diabetes in African Americans. To determine if differences in body composition and fat distribution explain race differences in insulin sensitivity and identify obesity measures that were independently associated with insulin sensitivity. Participants were 113 lean, overweight, and obese African-American and Caucasian-American adults without diabetes. Skeletal muscle insulin sensitivity was determined using a hyperinsulinemic-euglycemic clamp (SIClamp, insulin rate:120 mU/m2/min). Subcutaneous abdominal adipose tissue (SAAT), intra-abdominal adipose tissue (IAAT), and liver fat were measured by MRI; leg fat, total fat, and lean mass were measured by DXA. Race-by-adiposity interactions were significant in cross-sectional analyses utilizing multiple linear regression models for SIClamp (P<0.05); higher BMI, fat mass, SAAT, leg fat, and liver fat were associated with lower SIClamp in Caucasian Americans but not African Americans. Race-by-IAAT interaction was not significant (P=0.65). A central fat distribution (SAAT adjusted for leg fat) was associated with lower SIClamp in African Americans (β = -0.45, SE=0.11, P<0.001) but not Caucasian Americans (β = -0.42, SE=0.30, P=0.17). A peripheral fat distribution (leg fat adjusted for IAAT/SAAT) was associated with a higher SIClamp in African Americans (β = 0.11, SE=0.05, P=0.02) but lower SIClamp in Caucasian Americans (β = -0.28, SE=0.14, P=0.049). Lean mass was inversely associated with SIClamp in African Americans (β = -0.05, SE=0.03, P=0.04) but not Caucasian Americans (β = 0.08, SE=0.05, P=0.10) in the model for leg fat. Measures of overall adiposity were more strongly associated with SIClamp in Caucasian Americans, whereas body fat distribution and lean mass showed stronger correlations with SIClamp in African Americans. Insulin sensitivity may have a genetic basis in African Americans that is reflected in the pattern of body fat distribution. These findings suggest a race-specific pathophysiology of insulin resistance, which has implications for the prevention of diabetes and related cardiometabolic diseases.

The Role of Adiponectin in Maintaining Metabolic Homeostasis.

Adiponectin is an adipocyte-derived cytokine closely associated with obesity, altered body adipose tissue distribution, insulin resistance, and cardiovascular diseases. Evidence from animal and human studies demonstrate that adiponectin plays an important role in the regulation of glucose and lipid metabolism. Adiponectin increases insulin sensitivity and improves systemic lipid metabolism. Although research efforts on adiponectin mostly aim towards its endocrine functions, this adipocyte-derived molecule also has profound autocrine and paracrine functions. In this review, our aim is to discuss the role of adiponectin in maintaining metabolic homeostasis and its association with cardiovascular health. The proper identification of these roles is of great importance, which has the potential to identify a wealth of novel targets for the treatment of diabetes and related cardio-metabolic diseases.

Obesity-induced insulin resistance and macrophage infiltration of the adipose tissue: A vicious cycle.

Obesity-induced insulin resistance and macrophage infiltration of the adipose tissue: A vicious cycle.

Reprograming of Human Adipocytes to a Briter Phenotype—Enhanced Fatty Acid Oxidation and Lipid Droplet Remodeling

Converting energy storing white adipocytes to energy wasting ‘brite’ ones is now recognized to be feasible and may confer protection against obesity and its related cardiometabolic diseases. Fragments of omental and subcutaneous human adipose tissues were cultured for 7 days with insulin and dexamethasone with or without rosiglitazone (rosi) to induce britening. Rosi caused a metabolic reprograming of the adipocytes including increased rates of basal FA oxidation and the expression of mRNAs and proteins in multiple pathways that modulate FA metabolism, triacylglycerol synthesis, cellular FA trafficking, and mitochondrial oxidative capacity (PGC1a, UCP1, CIDEA, PLIN5, FABP3). Furthermore, these changes were associated with a dramatic remodeling of the surface of the adipocyte lipid droplet (LD) such that clusters of small LDs decorated with mitochondria were formed. Formation of these small LDs was blocked by inhibition of lipolysis and required FA activation and reesterification. Surprisingly, both omental and subcutaneous adipocytes were similarly ‘britened’. A similar remodeling was induced in primary cultures of newly-differentiated human adipocytes and these cells showed higher rates of basal and maximally-stimulated oxygen consumption. Consistent with transcriptome changes in both systems, lipidomics showed increased levels of unsaturated FAs, phospholipid species, and cardiolipins in brite cells. Taken together, these results identify a coordinated metabolic and structural reprogramming of mature human adipocytes toward a more oxidative phenotype. Although rosi has unacceptable clinical side effects, knowledge of the downstream effectors of this metabolic improvement may lead to development of targeted approaches to improve adipocyte and metabolic health and prevent type 2 diabetes in human obesity. Disclosure M. Lee: None. S. Jash: None. V. Puri: None. S.K. Fried: None.

Overweight and obesity management strategies in survivors of paediatric acute lymphoblastic leukaemia: a systematic review protocol

IntroductionAcute lymphoblastic leukaemia is the most common paediatric cancer. Survivors of childhood acute lymphoblastic leukaemia (SALL) are at risk of obesity and related cardiometabolic diseases including type 2 diabetes, hypertension,...

Household and familial resemblance in risk factors for type 2 diabetes and related cardiometabolic diseases in rural Uganda: a cross-sectional community sample

ObjectivesPrevention of type 2 diabetes (T2D) has been successfully established in randomised clinical trials. However, the best methods for the translation of this evidence into effective population-wide interventions remain unclear....