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The study was aimed to assess impact of high fat diet (HFD) and synthetic human gut microbiota (GM) combined with HFD and chow diet (CD) in inducing type-2 diabetes (T2D) using mice model. To our knowledge, this is the first study using selected human GM transplantation via culture based method coupled dietary modulation in mice for in vivo establishment of inflammation leading to T2D and gut dysbiosis. Twenty bacteria (T2D1-T2D20) from stool samples of confirmed T2D subjects were found to be morphologically different and subjected to purification on different media both aerobically and anerobically, which revealed seven bacteria more common among 20 isolates on the basis of biochemical characterization. On the basis of 16S rRNA gene sequencing, these seven isolates were identified as Bacteroides stercoris (MT152636), Lactobacillus acidophilus (MT152637), Lactobacillus salivarius (MT152638), Ruminococcus bromii (MT152639), Klebsiella aerogenes (MT152640), Bacteroides fragilis (MT152909), Clostridium botulinum (MT152910). The seven isolates were subsequently used as synthetic gut microbiome (GM) for their role in inducing T2D in mice. Inbred strains of albino mice were divided into four groups and were fed with CD, HFD, GM+HFD and GM+CD. Mice receiving HFD and GM+modified diet (CD/HFD) showed highly significant (P<0.05) increase in weight and blood glucose concentration as well as elevated level of inflammatory cytokines (TNF-α, IL-6, and MCP-1) compared to mice receiving CD only. The 16S rRNA gene sequencing of 11 fecal bacteria obtained from three randomly selected animals from each group revealed gut dysbiosis in animals receiving GM. Bacterial strains including Bacteroides gallinarum (MT152630), Ruminococcus bromii (MT152631), Lactobacillus acidophilus (MT152632), Parabacteroides gordonii (MT152633), Prevotella copri (MT152634) and Lactobacillus gasseri (MT152635) were isolated from mice [...].(AU)

O estudo teve como objetivo avaliar o impacto da dieta rica em gordura (HFD) e da microbiota intestinal humana sintética (GM) combinada com HFD e dieta alimentar (CD) na indução de diabetes tipo 2 (T2D) usando modelo de camundongos. Para nosso conhecimento, este é o primeiro estudo usando transplante de GM humano selecionado através do método baseado em cultura acoplada à modulação dietética em camundongos para o estabelecimento in vivo de inflamação que leva a T2D e disbiose intestinal. Vinte bactérias (T2D1-T2D20) de amostras de fezes de indivíduos T2D confirmados verificaram ser morfologicamente diferentes e foram submetidas à purificação em meios diferentes aerobicamente e anaerobicamente, o que revelou sete bactérias mais comuns entre 20 isolados com base na caracterização bioquímica. Com base no sequenciamento do gene 16S rRNA, esses sete isolados foram identificados como Bacteroides stercoris (MT152636), Lactobacillus acidophilus (MT152637), Lactobacillus salivarius (MT152638), Ruminococcus bromii (MT152639), Klebsiella aerogenides (MT152640), Bacteroides fragilis (MT152909), Clostridium botulinum (MT152910). Esses sete isolados foram, posteriormente, usados como microbioma intestinal sintético (GM) por seu papel na indução de T2D em camundongos. Linhagens consanguíneas de camundongos albinos foram divididas em quatro grupos e foram alimentadas com CD, HFD, GM + HFD e GM + CD. Camundongos que receberam a dieta modificada com HFD e GM + (CD / HFD) mostraram um aumento altamente significativo (P < 0,05) no peso e na concentração de glicose no sangue, bem como um nível elevado de citocinas inflamatórias (TNF-α, IL-6 e MCP-1) em comparação com os ratos que receberam apenas CD. O sequenciamento do gene 16S rRNA de 11 bactérias fecais obtidas de três animais selecionados aleatoriamente de cada grupo revelou disbiose intestinal em animais que receberam GM. Cepas bacterianas, incluindo Bacteroides gallinarum (MT152630), Ruminococcus [...].(AU)

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Human diabetic patients may have increased lactate levels compared to non-diabetics. Despite the use of lactate levels in critical care assessment, information is lacking for diabetic dogs. Therefore, this prospective cross-sectional clinical study aimed to determine lactate concentrations in 75 diabetic dogs [25 newly diagnosed non-ketotic diabetics, 25 under insulin treatment, and 25 in diabetic ketoacidosis (DKA)], compared to 25 non-diabetic dogs. Lactate levels (mmol/L) were not different among groups (P = 0.20); median and 25th to 75th percentile were 2.23 and P25-75 = 1.46 to 2.83 for controls, 1.69 and P25-75 = 1.09 to 2.40 for newly diagnosed non-ketotic diabetics, 2.27 and P25-75 = 1.44 to 2.90 for dogs under insulin treatment for at least 30 days, and 2.40 and P25-75 = 1.58 to 3.01 for dogs in DKA. Longitudinal studies assessing both isomers (L- and D-lactate) are needed to better elucidate the role of lactate in the pathophysiology of diabetes acid-base status in dogs.

La concentration de lactate de sang chez les chiens diabétiques. Des patients humains avec diabète peuvent présenter augmentation des niveaux de lactate, quand comparés aux non diabetiques. Bien que est utilisé d'évaluer les patients dans un état critique, cette information manque pour les chiens diabétiques. Par conséquent, cette étude clinique s'agit d'une prospective transversale en vue de detérminer les concentrations du lactate en 75 chiens diabétiques [25 au moment du diagnostic, 25 sous traitement à l'insuline et 25 dans l'acido-cétose diabétique (ACD)], par rapport aux 25 chiens non diabétiques. Les niveaux de L-lactate ne différaient pas entre les groupes (P = 0,20). Les valeurs médianes et les centiles 25 % et 75 % étaient de 2,23 mmol/L (P25­75 = 1,46 à 2,83) pour les contrôles, 1,69 mmol/L (P25­75 = 1,09 à 2,40) au diagnostic, 2,27 mmol/L (P25­75 = 1,44 à 2,90) sous traitement à l'insuline pendant au moins 30 jours, et 2,40 mmol/L (P25­75 = 1,58 à 3,01) dans ACD. Des études longitudinales évaluant les deux isomères (L et D-lactate) sont nécessaires pour élucider son rôle dans la physiopathologie et le déséquilibre acide-base chez les chiens diabétiques.(Traduit par Ana Carolina Possas Viana).

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There are several claims about the beneficial effects of supplementing L-glutamine to both type 1 and type 2 diabetes. The purpose of the present study was to provide detailed knowledge about the fate of this amino acid in the liver, the first organ that receives the compound when ingested orally. The study was done using the isolated perfused rat liver, an experimental system that preserves the microcirculation of the organ and that allows to measured several parameters during steady-state and pre steady-state conditions. L-Glutamine was infused in the portal vein (5 mM) and several parameters were monitored. Livers from type 1 diabetic rats showed an accelerated response to L-glutamine infusion. In consequence of this accelerated response livers from type 1 diabetic rats presented higher rates of ammonia, urea, glucose and lactate output during the first 25-30 minutes following L-glutamine infusion. As steady-state conditions approached, however, the difference between type 1 diabetes and control livers tended to disappear. Measurement of the glycogen content over a period of 100 minutes revealed that, excepting the initial phase of the L-glutamine infusion, the increased glucose output in livers from type 1 diabetic rats was mainly due to accelerated glycogenolysis. Livers from type 2 diabetic rats behaved similarly to control livers with no accelerated glucose output but with increased L-alanine production. L-Alanine is important for the pancreatic ß-cells and from this point of view the oral intake of L-glutamine can be regarded as beneficial. Furthermore, the lack of increased glucose output in livers from type 2 diabetic rats is consistent with observations that even daily L-glutamine doses of 30 g do not increase the glycemic levels in well controlled type 2 diabetes patients.

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