The role of very-low-carbohydrate ketogenic diets (VLCKD) in the long-term management of obesity is not well established. The present meta-analysis aimed to investigate whether individuals assigned to a VLCKD (i.e. a diet with no more than 50 g carbohydrates/d) achieve better long-term body weight and cardiovascular risk factor management when compared with individuals assigned to a conventional lowfat diet (LFD; i.e. a restricted-energy diet with less than 30 % of energy from fat). Through August 2012, MEDLINE, CENTRAL, ScienceDirect, Scopus, LILACS, SciELO, ClinicalTrials.gov and grey literature databases were searched, using no date or language restrictions, for randomised controlled trials that assigned adults to a VLCKD or a LFD, with 12 months or more of follow-up. The primary outcome was body weight. The secondary outcomes were TAG, HDL-cholesterol (HDL-C), LDL-cholesterol (LDL-C), systolic and diastolic blood pressure, glucose, insulin, HbA 1c and C-reactive protein levels. A total of thirteen studies met the inclusion/exclusion criteria. In the overall analysis, five outcomes revealed significant results. Individuals assigned to a VLCKD showed decreased body weight (weighted mean difference 20·91 (95 % CI 2 1·65, 20·17) kg, 1415 patients), TAG (weighted mean difference 2 0·18 (95 % CI 20·27, 2 0·08) mmol/l, 1258 patients) and diastolic blood pressure (weighted mean difference 2 1·43 (95 % CI 22·49, 2 0·37) mmHg, 1298 patients) while increased HDL-C (weighted mean difference 0·09 (95 % CI 0·06, 0·12) mmol/l, 1257 patients) and LDL-C (weighted mean difference 0·12 (95 % CI 0·04, 0·2) mmol/l, 1255 patients). Individuals assigned to a VLCKD achieve a greater weight loss than those assigned to a LFD in the long term; hence, a VLCKD may be an alternative tool against obesity.Key words: Cardiovascular risk factors: Low-carbohydrate diets: Meta-analysis: Obesity: Weight loss Obesity continues to be a major worldwide health problem, despite the efforts of the medical community. At least 2·8 million adults die from obesity-related causes each year, and 65 % of the worldwide population lives in countries where obesity causes more deaths than underweight (1) . Although it is a difficult task, intensive lifestyle interventions can achieve weight loss that is sustained over the long term, as shown by the findings of a recent large clinical trial (2) .Diet is a cornerstone of any lifestyle intervention programme. The dietary plan that restricts energy and fat is the most common strategy, and based on it, several other dietary strategies have been proposed (3 -5) . The very-low-carbohydrate ketogenic diet (VLCKD) differs from these approaches. According to Accurso et al. A major concern regarding the prescription of the VLCKD is the adherence of the individuals assigned to it, since it promotes important lifestyle changes (7) . Given the importance of dietary counselling in weight loss, it is useful to investigate the effectiveness of different dietary therapies. A recent large randomised clinical trial, whic...

RESUMOOs produtos finais da glicação avançada (AgEs [do inglês, Advanced Glycation End-products]) constituem uma classe de moléculas heterogêneas formadas a partir de reações aminocarbonilo de natureza não-enzimática, que ocorrem aceleradamente no estado hiperglicêmico do diabetes. considerados importantes mediadores patogênicos das complicações diabéticas, os AgEs são capazes de modificar, irreversivelmente, as propriedades químicas e funcionais das mais diversas estruturas biológicas. na presente revisão, são apresentados os dados recentes da literatura que descrevem as vias de formação de AgEs, seu metabolismo, os principais mecanismos de ação dessas substâncias no desencadeamento dos processos patológicos, bem como os méto-dos de determinação de AgEs em amostras biológicas. Este artigo aponta, ainda, novas perspectivas de terapias anti-AgEs, a exemplo de estudos envolvendo a ação de compostos naturais dos alimentos, que podem oferecer potencial terapêutico para os portadores de diabetes ou de outras patologias associadas ao acúmulo degenerativo de AgEs. the advanced glycation end-products (AgEs) constitute a class of heterogeneous molecules formed by amino-carbonyl reactions of a non-enzymatic nature, which occur at an accelerated rate in the hyperglycemic state of diabetes. considered important pathogenic mediators of diabetic complications, AgEs are capable of irreversibly modifying the chemical properties and functions of diverse biological structures. In this review, recent data from literature is presented describing the pathways of AgEs formation, their metabolism, the main mechanisms of action of these substances in the triggering of pathological processes associated with diabetes, as well as methods of AgEs determination in biological samples. this text also points to new perspectives in anti-AgE therapies, an example of which is the studies involved with the action of natural compounds of food, which can represent a potential coadjuvant therapy for people with diabetes or other pathologies associated with the degenerative accumulation of AgEs.

No abstract

A geração dos produtos de glicação avançada é um dos principais mecanismos desencadeadores das doenças associadas ao diabetes mellitus, que incluem cardiopatia, retinopatia, neuropatia e nefropatia. Esta revisão tem como objetivo analisar o papel dos produtos de glicação avançada presentes na alimentação como mediadores das complicações diabéticas e apresentar estratégias de redução de sua ingestão. Para tanto, foram realizados levantamentos em bancos de dados de publicações da área, dos últimos 15 anos, considerando-se artigos de revisão, estudos clínicos e experimentais. Os produtos de glicação avançada são um grupo heterogêneo de moléculas formadas a partir de reações não enzimáticas entre grupamentos amino e carbonilo, sendo a carboximetilisina e a pentosidina exemplos de produtos de glicação avançada identificados em alimentos e in vivo. Os produtos de glicação avançada ingeridos são absorvidos, somando-se aos endógenos no surgimento e na progressão das diversas complicações do diabetes, existindo uma correlação direta entre o consumo e a concentração sanguínea. Sua restrição na alimentação se correlaciona à supressão dos níveis séricos de marcadores de doença vascular e de mediadores inflamatórios diretamente envolvidos no desenvolvimento das degenerações diabéticas. As atuais orientações dietéticas centram-se na proporção em nutrientes e na restrição energética, sem considerar o risco da ingestão de produtos de glicação avançada formados durante o processamento dos alimentos. Recomendações simples, como a utilização de temperaturas baixas por períodos mais curtos, em presença de água, no preparo de alimentos, exercem efeitos importantes na prevenção das complicações do diabetes. O estudo dos mecanismos envolvidos na geração de produtos de glicação avançada e das propriedades anti-glicação de compostos presentes nos alimentos podem contribuir com a conduta terapêutica, concorrendo para a melhoria da qualidade de vida dos portadores dessa enfermidade. Termos de indexação:Diabetes mellitus. Dieta. Produtos finais de glicosilação.

Chronic energy restriction, a-tocopherol supplementation and their interaction with exhaustive exercise were investigated. Eleven-week-old male Wistar rats ðn 6 £ 10Þ were fed either a control (C ), a 30 % carbohydrate-energy-restricted control (R ) or an a-tocopherol-supplemented (S ) diet for 5 months. The animals in each diet were divided into exercised (E ) and non-exercised (NE ) groups. Before killing, the exercised rats were required to run to exhaustion (39 (SE 6), 69 (SE 11) and 18 (SE 2) min for the C, R and S groups, respectively). Lipid peroxidation (thiobarbituric acid-reactive substances; TBARS), protein damage (reactive carbonyls) and atocopherol were determined in gastrocnemius, liver, brain and/or plasma. There was no difference in lipid peroxidation between the R and C groups, but in liver and muscle peroxidation appeared significantly lower in the S than the other two diets. TBARS in the brain were similar in all groups. On the other hand, reactive carbonyls showed that both the R and S diets reduced protein damage in the brain, while exhaustive exercise increased it. For liver and muscle, however, reactive carbonyl levels were similar in all groups. a-Tocopherol supplementation increased the vitamin concentrations in liver, muscle and plasma, but exercise decreased them in plasma and brain. Carbohydrate-energy restriction increased (P¼ 0·0025) resistance to exhaustive exercise considerably without depleting stores of a-tocopherol or exacerbating oxidative damage in monitored tissues. It is concluded that while exhaustive exercise promotes a tissue-specific oxidative damage detectable only in brain proteins, both experimental diets tended to ameliorate this condition.