Obesity frequently co-exists with type 2 diabetes mellitus (T2DM), leading to the socalled "diabesity epidemic". The metabolic syndrome (MetS), a cluster of central obesity, hypertension, ...dysglycemia, insulin resistance and/or atherogenic dyslipidemia, as well as non-alcoholic fatty liver disease (NAFLD), a hepatic manifestation of MetS, has been associated with increased cardiovascular disease (CVD), T2DM and chronic kidney disease (CKD) incidence. However, the association between obesity, MetS (including NAFLD) and diabetic microvascular complications is less evident.
The present narrative review discusses the associations of obesity, MetS and NAFLD with diabetic kidney disease (DKD), diabetic retinopathy (DR) and diabetic peripheral neuropathy (DPN) as well as cardiac autonomic neuropathy (CAN). The available data on the effects of lifestyle measures and bariatric surgery on these diabetic complications are also briefly discussed.
Overall, both obesity and MetS have been related to DKD, DR and DPN, although conflicting results exist. Links between NAFLD and diabetic microvascular complications have also been reported but data are still limited. Lifestyle intervention and bariatric surgery may prevent the development and/or progression of these microvascular complications but more evidence is needed.
Clinicians should be aware of the frequent co-existence of MetS and/or NAFLD in T2DM patients to prevent or treat these metabolic disorders, thus potentially minimizing the risk for both CVD and diabetic microvascular complications.
A systematic literature review was conducted using PubMed, Embase and the Cochrane Library to determine the effect of acute, chronic and passive smoking on arterial stiffness and to determine whether ...these effects are reversible after smoking cessation. A total of 39 relevant studies were identified and included. Acute smoking was found to cause an acute increase in arterial stiffness. Similarly, passive smoking increased arterial stiffness acutely and chronically. The majority of studies identified chronic smoking as a risk factor for increasing arterial stiffness. However, some studies found no statistical difference in arterial stiffness between nonsmokers and long-term smokers, although chronic smoking seems to sensitize the arterial response to acute smoking. In addition, whether arterial stiffness is reversed after smoking cessation and the timeline in which this may occur could not be determined from the identified literature. The effect of smoking discontinuation on arterial stiffness remains to be established by prospective smoking cessation trials.
Increased epicardial fat deposition has been associated with type 2 diabetes mellitus (T2DM) and cardiovascular disease (CVD),2,3 as well as with the presence and severity of non-alcoholic fatty ...liver disease (NAFLD).4 A study reported that South Asians (n = 50) and Southeast or East Asians (n = 50) had significantly greater epicardial fat volume (measured by computed-tomographic-coronary-angiography) than Caucasians (n = 50).5 However, another study compared 803 South Asians from the Mediators of Atherosclerosis in South Asians Living in America (MASALA) study with 2622 whites, 1893 African Americans, 1496 Latinos, and 803 Chinese Americans from the Multi-Ethnic Study of Atherosclerosis (MESA) study and found that South Asians had the lowest pericardial fat volume (PFV) but the highest intrahepatic fat.6 Of note, PFV was independently associated with coronary artery calcium severity only in South Asians and African Americans.6 In another cross-sectional analysis of these 2 community-based cohorts (i.e., MASALA and MESA), South Asians (n = 906) had a significantly greater amount of pericardial fat compared with African Americans (n = 1893).7 Non-alcoholic fatty pancreas disease (NAFPD) is also related to NAFLD, T2DM and CVD risk.8 Only a few studies evaluated racial/ethnic differences in relation to NAFPD. South Asians have a greater risk for T2DM and CVD.11,12 Indeed, migrant South Asians living in high-income countries have been reported to be more insulin resistant than white Europeans, potentially experiencing pancreatic beta cell exhaustion at a younger age.11 As a consequence, South Asians may develop T2DM 5–10 years earlier than whites and at a lower BMI.11 Epigenetic factors may play a major role.11,13 However, a polygenic risk score was recently reported to predict a ~4-fold higher T2DM risk in South Asians.14 Furthermore, differences in skeletal muscle (low cardiorespiratory fitness and lean mass percentage) and adipose depots (increased body fat, SAT and visceral fat) were reported to affect this risk.11,15 In this context, the recent finding that South Asians accumulate more liver fat, as discussed above,1 further contributes to these associations. MR has given lectures, received honoraria and research support, and participated in conferences, advisory boards and clinical trials sponsored by many pharmaceutical companies, including Amgen, Astra Zeneca, Boehringer Ingelheim, Kowa, Eli Lilly, Meda, Mylan, Merck Sharp & Dohme, Novo Nordisk, Novartis, Roche Diagnostics, Sanofi and Servier.
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Recently, concerns regarding the safety of red yeast rice (RYR) have been raised after the publication of some case reports claiming toxicity. Since the previous meta-analyses on the ...effects of RYR were mainly focused on its efficacy to improve lipid profile and other cardiovascular parameters, we carried out a meta-analysis on safety data derived from the available randomized controlled clinical trials (RCTs).
Primary outcomes were musculoskeletal disorders (MuD). Secondary outcomes were non-musculoskeletal adverse events (Non-MuD) and serious adverse events (SAE). Subgroups analyses were carried out considering the intervention (RYR alone or in association with other nutraceutical compounds), monacolin K administered daily dose (≤3, 3.1–5 or >5 mg/day), follow-up (>12 or ≤12 weeks), with statin therapy or statin-intolerance and type of control treatment (placebo or statin treatment).
Data were pooled from 53 RCTs comprising 112 treatment arms, which included 8535 subjects, with 4437 in the RYR arm and 4303 in the control one. Monacolin K administration was not associated with increased risk of MuD (odds ratio (OR) = 0.94, 95% confidence interval (CI) 0.53,1.65). Moreover, we showed reduced risk of Non-MuD (OR = 0.59, 95%CI 0.50, 0.69) and SAE (OR = 0.54, 95%CI 0.46, 0.64) vs. control. Subgroups analyses confirmed the high tolerability profile of RYR. Furthermore, increasing daily doses of monacolin K were negatively associated with increasing risk of Non-MuD (slope: -0.10; 95%CI: -0.17, -0.03; two-tailed p < 0.01).
Based on our data, RYR use as lipid-lowering dietary supplement seems to be overall tolerable and safe in a large kind of moderately hypercolesterolaemic subjects.
Summary Background Long-term statin treatment reduces the frequency of cardiovascular events, but safety and efficacy in patients with abnormal liver tests is unclear. We assessed whether statin ...therapy is safe and effective for these patients through post-hoc analysis of the Greek Atorvastatin and Coronary Heart Disease Evaluation (GREACE) study population. Methods GREACE was a prospective, intention-to-treat study that randomly assigned by a computer-generated randomisation list 1600 patients with coronary heart disease (aged <75 years, with serum concentrations of LDL cholesterol >2·6 mmol/L and triglycerides <4·5 mmol/L) at the Hippokration University Hospital, Thessaloniki, Greece to receive statin or usual care, which could include statins. The primary outcome of our post-hoc analysis was risk reduction for first recurrent cardiovascular event in patients treated with a statin who had moderately abnormal liver tests (defined as serum alanine aminotransferase or aspartate aminotransferase concentrations of less than three times the upper limit of normal) compared with patients with abnormal liver tests who did not receive a statin. This risk reduction was compared with that for patients treated (or not) with statin and normal liver tests. Findings Of 437 patients with moderately abnormal liver tests at baseline, which were possibly associated with non-alcoholic fatty liver disease, 227 who were treated with a statin (mainly atorvastatin 24 mg per day) had substantial improvement in liver tests (p<0·0001) whereas 210 not treated with a statin had further increases of liver enzyme concentrations. Cardiovascular events occurred in 22 (10%) of 227 patients with abnormal liver tests who received statin (3·2 events per 100 patient-years) and 63 (30%) of 210 patients with abnormal liver tests who did not receive statin (10·0 events per 100 patient-years; 68% relative risk reduction, p<0·0001). This cardiovascular disease benefit was greater (p=0·0074) than it was in patients with normal liver tests (90 14% events in 653 patients receiving a statin 4·6 per 100 patient-years vs 117 23% in 510 patients not receiving a statin 7·6 per 100 patient-years; 39% relative risk reduction, p<0·0001). Seven (<1%) of 880 participants who received a statin discontinued statin treatment because of liver-related adverse effects (transaminase concentrations more than three-times the upper limit of normal). Interpretation Statin treatment is safe and can improve liver tests and reduce cardiovascular morbidity in patients with mild-to-moderately abnormal liver tests that are potentially attributable to non-alcoholic fatty liver disease. Funding None.
Uric acid and diabetes: Is there a link? Katsiki, Niki; Papanas, Nikolaos; Fonseca, Vivian A ...
Current pharmaceutical design,
2013, Letnik:
19, Številka:
27
Journal Article
Recenzirano
Elevated serum uric acid (SUA) levels (i.e. hyperuricaemia) have been associated with metabolic syndrome (MetS) and cardiovascular disease (CVD) morbidity and mortality. Elevated SUA levels predict ...the onset of type 2 diabetes (T2DM). SUA levels are increased during the early stages of impaired glucose metabolism. Furthermore, in diabetic patients, hyperuricaemia has been linked to both micro- and macrovascular complications. The present review considers: (1) SUA levels in patients with MetS, type 1 diabetes and T2DM; (2) the mechanisms that influence SUA levels in these patients; (3) the potential links between SUA and diabetic complications. The effect on SUA levels of drugs commonly prescribed for T2DM and the risk of uric acid nephrolithiasis in patients with MetS or DM are also briefly discussed.
Small, dense low density lipoprotein (sdLDL) represents an emerging cardiovascular risk factor, since these particles can be associated with cardiovascular disease (CVD) independently of established ...risk factors, including plasma lipids. Obese subjects frequently have atherogenic dyslipidaemia, including elevated sdLDL levels, in addition to elevated triglycerides (TG), very low density lipoprotein (VLDL) and apolipoprotein-B, as well as decreased high density lipoprotein cholesterol (HDL-C) levels. Obesity-related co-morbidities, such as metabolic syndrome (MetS) are also characterized by dyslipidaemia. Therefore, agents that favourably modulate LDL subclasses may be of clinical value in these subjects. Statins are the lipid-lowering drug of choice. Also, anti-obesity and lipid lowering drugs other than statins could be useful in these patients. However, the effects of anti-obesity drugs on CVD risk factors remain unclear. We review the clinical significance of sdLDL in being overweight and obesity, as well as the efficacy of anti-obesity drugs on LDL subfractions in these individuals; a short comment on HDL subclasses is also included. Our literature search was based on PubMed and Scopus listings. Further research is required to fully explore both the significance of sdLDL and the efficacy of anti-obesity drugs on LDL subfractions in being overweight, obesity and MetS. Improving the lipoprotein profile in these patients may represent an efficient approach for reducing cardiovascular risk.
Background and aim: Growing evidence suggests that some of the effects of diet on cardiovascular disease (CVD) occur through mechanisms involving subclinical inflammation. We assessed the ...relationship between selected dietary constituents and serum high-sensitivity C-reactive protein (hsCRP) concentration in a population-based sample of United States adults.
Methods: In this cross-sectional analysis, participants were selected from the US National Health and Nutrition Examination Survey (NHANES) and restricted to those with available data on dietary intake, biochemical and anthropometric measurements from 2001 to 2010. All statistical analyses accounted for the survey design and sample weights by using SPSS Complex Samples v22.0 (IBM Corp, Armonk, NY).
Results: Of the 17,689 participants analysed, 8607 (48.3%) were men. The mean age was 45.8 years in the overall sample, 44.9 in men and 46.5 in women (p = .047). The age-, race-, sex-, energy intake- and body mass index-adjusted mean dietary intakes of total dietary fibre, polyunsaturated fatty-acids, vitamin E, vitamin A, vitamin B6, total folate, vitamin B family, vitamin C, vitamin K, magnesium, iron, copper and potassium monotonically decreased across increasing hsCRP quarters (p < .001 for all), whereas sugar intake increased (p < .001). In analysis of covariance adjusted for potential confounders (age-, race-, sex-, energy intake- and body weight-) hsCRP levels increased across increasing quarters of sugar intake (p < .001).
Conclusions: This study provides further evidence of an association between dietary sugar, polyunsaturated fatty-acids, fibre and antioxidant intake and hsCRP levels, a subclinical inflammation marker. hsCRP concentrations are likely modulated by dietary intake.
KEY MESSAGES
Serum high-sensitivity C-reactive protein (hsCRP) concentration is positively associated with sugar intake, and negatively with the consumption of minerals, vitamins and polyunsaturated fatty-acids (fruit and vegetables).
hsCRP concentrations, and accordingly subclinical inflammation, are likely influenced by dietary intake.
An Expert Panel group of scientists and clinicians met to consider several aspects related to non-fasting and postprandial triglycerides (TGs) and their role as risk factors for cardiovascular ...disease (CVD). In this context, we review recent epidemiological studies relevant to elevated non-fasting TGs as a risk factor for CVD and provide a suggested classification of non-fasting TG concentration. Secondly, we sought to describe methodologies to evaluate postprandial TG using a fat tolerance test (FTT) in the clinic. Thirdly, we discuss the role of non-fasting lipids in the treatment of postprandial hyperlipemia. Finally, we provide a series of clinical recommendations relating to non-fasting TGs based on the consensus of the Expert Panel: 1). Elevated non-fasting TGs are a risk factor for CVD. 2). The desirable non-fasting TG concentration is <2 mmol/l (<180 mg/dl). 3). For standardized postprandial testing, a single FTT meal should be given after an 8 h fast and should consist of 75 g of fat, 25 g of carbohydrates and 10 g of protein. 4). A single TG measurement 4 h after a FTT meal provides a good evaluation of the postprandial TG response. 5). Preferably, subjects with non-fasting TG levels of 1-2 mmol/l (89-180 mg/dl) should be tested with a FTT. 6). TG concentration ≤ 2.5 mmol/l (220 mg/dl) at any time after a FTT meal should be considered as a desirable postprandial TG response. 7). A higher and undesirable postprandial TG response could be treated by aggressive lifestyle modification (including nutritional supplementation) and/or TG lowering drugs like statins, fibrates and nicotinic acid.
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