Suzana Lima de Oliveira

Very-low-carbohydrate ketogenic diet v. low-fat diet for long-term weight loss: a meta-analysis of randomised controlled trials

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 low-fat 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 bodyweight. The secondary outcomes were TAG, HDL-cholesterol (HDL-C), LDL-cholesterol (LDL-C), systolic and diastolic blood pressure,glucose, insulin, HbA1c 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 -0·91 (95% CI -1·65, -0·17) kg, 1415 patients), TAG (weighted mean difference -0·18 (95% CI -0·27, -0·08) mmol/l, 1258 patients)and diastolic blood pressure (weighted mean difference -1·43 (95% CI -2·49, -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 longterm; hence, a VLCKD may be an alternative tool against obesity.

Effects of short-term and long-term treatment with medium- and long-chain triglycerides ketogenic diet on cortical spreading depression in young rats.

The ketogenic diet (KD) is a high fat and low carbohydrate and protein diet. It is used in the clinical treatment of epilepsy, in order to decrease cerebral excitability. KD is usually composed by long-chain triglycerides (LCT) while medium-chain triglycerides (MCT) diet is beginning to be used in some clinical treatment of disorders of pyruvate carboxylase enzyme and long-chain fatty acid oxidation. Our study aimed to analyze the effects of medium- and long-chain KD on cerebral electrical activity, analyzing the propagation of the phenomenon of cortical spreading depression (CSD). Three groups of weaned rats (21 days old) received, for 7 weeks, either a control (AIN-93G diet), or a MCT-KD (rich in triheptanoin oil), or a LCT-KD (rich in soybean oil). They were compared to another three groups (21 days old) receiving the same diets for just 10 days. CSD propagation was evaluated just after ending the dietary treatments. Results showed that short-term KD treatment resulted in a significant reduction of the CSD velocity of propagation (control group: 4.02+/-1.04mm/min; MCT-KD: 0.81+/-1.46mm/min and LCT-KD: 2.26+/-0.41mm/min) compared to the control group. However, long-term treatment with both KDs had no effect on the CSD velocity (control group: 3.10+/-0.41mm/min, MCT-KD: 2.91+/-1.62mm/min, LCT-KD: 3.02+/-2.26mm/min) suggesting that both short-term KDs have a positive effect in decreasing brain cerebral excitability in young animals. These data show for the first time that triheptanoin has an effect on central nervous system.

O Papel dos Produtos Finais da Glicação Avançada (AGEs) no Desencadeamento das Complicações Vasculares do Diabetes revisão

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.

Produtos da glicação avançada dietéticos e as complicações crônicas do diabetes

The generation of advanced glycation end products is one of the principal mechanisms that lead to the pathologies associated with diabetes mellitus, which include cardiopathy, retinopathy, neuropathy and nephropathy. The objective of this revision is to analyse the role of the advanced glycation end products present in food as intermediaries of diabetic complications, presenting strategies to reduce their ingestion. For this purpose, research was carried out in databases of publications of the area, for the last 15 years, taking into account revision, experimental and clinical studies. Advanced glycation end products are a heterogenous group of molecules coming from non-enzymatic reactions between amino and carbonyl groups, examples being carboxymethyllisine and pentosidine found in food and in vivo. The advanced glycation end products ingested are absorbed and, along with endogenous advanced glycation end-products, promote the progression of the complications of diabetes. There is a direct correlation between advanced glycation end products consumption and blood concentration. Their restriction in food results in the suppression of serum levels of the markers of vascular disease and the intermediaries of inflammation directly involved in the development of diabetic degenerations. The current dietary orientations are concentrated on the proportion of nutrients and on energetic restriction. The risk of ingestion of advanced glycation end products formed during the processing of food should be taken in consideration. It is simply recommended that in the preparation of food, the use of low temperatures for short periods, in the presence of water, has important effects in the prevention of the complications of diabetes. The study of the mechanisms involved in the generation of advanced glycation end products and the antiglycation properties of compounds presented in foods can contribute to a therapeutic practice and an improvement in the quality of life of people with this disease.

Hepatoprotective effect of diheptanoin and tritreptanoin chronic consumption against steatosis in rats

OBJECTIVE To evaluate the effect of chronic consumption of di- and triheptanoin on hepatic steatosis (HS) in rats. METHODOLOGY Wistar rats were submitted to a diet AIN-93 with 0, 30 or 50% of its oil substituted with an oil rich in di- and triheptanoin, groups TAGC(7)0, TAGC(7)30 and TAGC(7)50 respectively, for nine months. The control group received Labina(R). Liver histology, hepatic lesion and function proofs, glycemia and lipid profile, were performed. Variance analyses, F-test, Dunnet s test and uni- and multivariate regression analyses were performed (p<0.05). RESULTS TAGC(7)0, TAGC(7)30 and TAGC(7)50 developed HS; 80% of severe cases in TAGC(7)0, as against 40% in TAGC(7)50. The absolute (ALW) and relative (RLW) liver weights were higher in TAGC(7)0 and TAGC(7)30, and glycemia was greater in TAGC(7)30 and TAGC(7)50, than in the Control. Total cholesterol, LDL-c, LDL-c/HDL-c and total proteins were higher in the Control. The experimental oil reduced RLW and showed a tendency in the reduction of body weight, ALW, percentage of hepatic lipids and the severity of HS. The explanatory variables in relation to HS were final weight, glycemia, albumin, HDL-c, LDL-c, LDL-c/HDL-c, VLDL-c and alkaline phosphatase. CONCLUSIONS It is suggested that di- and triheptanoin have a hepatoprotector effect against HS, in rats, in a dose-dependent manner.

LA INGESTA DE LA DIETA ESTÁNDAR AIN-93 INDUCE ESTEATOSIS HEPÁTICA CON ALTERADO PERFIL DE ÁCIDOS GRASOS EN RATONES WISTAR

BACKGROUND There are several standard diets for animals used in scientific research, usually conceived by scientific institutions. The AIN-93 diet is widely used, but there are some reports of fatty liver in Wistar rats fed this diet. OBJECTIVE We aimed to evaluate the hepatic repercussions of the AIN-93 diet intake in Wistar rats. METHODS Forty newly-weaned 21-day-old male Wistar rats were fed either the AIN-93 diet or a commercial diet for either 1 month or 4 months. Weight gain, serum biochemistry, hepatic histology, and hepatic fatty acid profile were analyzed. RESULTS Hepatic steatosis was observed, especially in the group fed the AIN-93 diet. Serum blood glucose, absolute and relative liver weight and hepatic levels of oleic, palmitoleic, stearic, and palmitic fatty acids were related to the observed steatosis, while lipidogram and serum markers of liver function and injury were not. CONCLUSION AIN-93 diet induced acute hepatic steatosis in Wistar rats, which may compromise its use as a standard diet for experimental studies with rodents. The hepatic fatty acid profile was associated with steatosis, with possible implications for disease prognosis.

O papel da dieta cetogênica no estresse oxidativo presente na epilepsia experimental

INTRODUCTION: Epilepsy is a neurological disorder more common, being defined as a condition of spontaneous recurrent seizures. An important relationship exists between free radicals and antioxidant enzymes in epileptic phenomena and reactive oxygen species (ROS) have been implicated in neurodegeneration induced by crises. AIM: This review aimed to investigate the relationship between oxidative stress and epilepsy, highlighting the effect of the ketogenic diet under experimental conditions. METHODS: There has been research papers published in the databases Medline, PubMed, CAPES journals, ScienceDirect and Scielo. The keywords selected for the study included epilepsy, status epilepticus, pilocarpine, oxidative stress, reactive oxygen species, mitochondrial dysfunction. RESULTS AND DISCUSSION: Dietary therapy has been used, such as the ketogenic diet (KD), which is rich in fat and low in carbohydrates and used by more than eight decades for the treatment of refractory epilepsy, especially in children. The KD modulates mitochondrial bioenergetic, decreases the formation of ROS, increases the antioxidant capacity and also prevents changes in mitochondrial DNA. CONCLUSION: Evidence of activity of KD in mitochondrial dysfunction, as epilepsy, are many and clearly demonstrate the beneficial effects of the therapy.

Hepatic fatty acid profile of rats with AIN-93 diet-induced steatosis attenuated by the partial substitution of soybean oil by diheptanoin and triheptanoin

Nassib Bezerra BuenoLaboratorio de Nutricao Experimental, Faculdade de Nutricao, Universidade Federal de Alagoas, UFAL, Campus A. C. Simoes, Cidade Universitaria, BR 104 Norte, Km 97 57.072-970 – Tabuleiro dos Martins, Maceio, Brasil nassibbb@hotmail.comRecebido em 12/Fev/2010Aceito em 25/Maio/2010

Hepatic fatty acid profile of rats fed a triheptanoin-based ketogenic diet

OBJECTIVE the aim of this study was to evaluate the influence of consumption of a ketogenic diet supplemented with triheptanoin, a medium-chain anaplerotic triacylglycerol, on the liver fatty acid profile of Wistar rats. METHODS three groups of male Wistar rats (n = 10) were submitted to an AIN-93 control diet, a triheptanoin- based ketogenic diet, or a soybean oil-based ketogenic diet for 60 days. Excised livers were subjected to lipid extraction and methylation to obtain fatty acids methyl esters, which were subjected to gas chromatography- mass spectrometry. RESULTS AND DISCUSSION compared to the rats fed the control diet, those fed ketogenic diets showed a significant reduction in the concentrations of 9-hexadecenoic and 9-octadecenoic acids, whereas those fed triheptanoin showed increased levels of octadecanoic acid. CONCLUSION changes in the liver fatty acid profiles of the rats fed a triheptanoin-based or a soybean oil-based ketogenic diet did not seem to be related to the dietary fat source, but rather to the characteristics of the ketogenic diets themselves.

Malnutrition and experimental epilepsy

INTRODUCAO: Perturbacoes ao ambiente intrauterino podem ter efeitos prejudiciais sobre o feto e consequencias patologicas persistentes ao longo da adolescencia e da idade adulta. Restricao proteica durante o periodo pre-natal tem repercussoes significativas sobre a ontogenia e o desenvolvimento do sistema nervoso central. Restricao alimentar nessa fase da vida aumenta o risco de disturbios neurologicos como a epilepsia. OBJETIVO: Relacionar o modelo de programacao pela desnutricao e suas implicacoes na epilepsia experimental. MATERIAL E METODOS: Procedeu-se a pesquisa em artigos cientificos publicados nos Bancos de Dados Medline, PubMed, Periodicos CAPES, ScienceDirect e Scielo. As palavras-chave selecionadas para a pesquisa incluiram epilepsia, status epilepticus, pilocarpina, desnutricao, programming. RESULTADOS E DISCUSSAO: Diversos estudos realizados em modelos animais ou humanos destacam os possiveis efeitos adversos da desnutricao no inicio das crises epilepticas. A vulnerabilidade imunologica, alteracoes bioquimicas como anormalidades eletroliticas e hipoglicemia podem ser os fatores responsaveis pela intensificacao dos processos epileptogenicos em individuos desnutridos. Conclusao: A desnutricao altera negativamente a circuitaria epileptogenica.