Ketogenesis evaluation in perfused liver of diabetic rats submitted to short‐term insulin‐induced hypoglycemia

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Blood metabolic parameters of Walker-256 tumour-bearing rats, on days 5, 8, 11 and 14 after implantation of tumour, were compared with those of rats without tumour fed ad libitum (free-fed control) or with reduced feeding (pair-fed control), similar to the anorexic tumour-bearing rats. Cachexia parameters and tumour mass also were investigated. In general, especially on day 14 after implantation of tumour, there was reduction of body mass, gastrocnemius muscle mass, food intake and glycemia and increase of blood triacylglycerol, free fatty acids, lactate and urea, compared with free-fed controls rats. These changes did not occur in pair-fed control, except a slight reduction of glycemia. Pair-fed control showed no significant changes in blood cholesterol and glycerol in comparison with free-fed control, although there was reduction of cholesterol and increase of blood glycerol on day 14 after tumour implantation compared with pair-fed control. The results demonstrate that, besides the characteristic signs of the cachexia syndrome such as anorexia, weight loss and muscle catabolism, Walker-256 tumour-bearing rats show several blood metabolic alterations, some of which begin as early as day 5 after implantation of tumour, and are accentuated during the development of cachexia. Evidence that the alterations of blood metabolic parameters of tumour-bearing rats were not found in pair-fed control indicate that they were not caused by decreased food intake. These changes were probably mediated by factors produced by tumour or host tissue in response to the presence of tumour.

“…Total cholesterol, glucose, lactate and urea were assayed using standard enzymatic methods, as previously described . FFA was determined by the method of Falholt .…”

Section: Methodsmentioning

confidence: 99%

Changes in blood metabolic parameters during the development of Walker‐256 tumour‐induced cachexia in rats are not caused by decreased food intake

Cassolla

Moreira

Liboni

et al. 2011

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“…19,20,34 Furthermore, the reason for using this medium-chain fatty acid was based on the following facts: high solubility in water; transport through the mitochondrial membrane does not require a carnitinedependent transport mechanism; and exclusively metabolised by mitochondria and higher capacity to produce ketone bodies compared with other fatty acids. To evaluate hepatic ketogenesis, livers were infused with a constant and saturating concentration of octanoate, i.e.…”

Section: Discussionmentioning

confidence: 99%

“…19,20 A demonstrative experiment, shown in Figure 1, in which after a pre-infusion period (10 min), the gluconeogenic substrate was dissolved in Krebs-Henseleit buffer and infused over 30 min, followed by a post-infusion period (10 min without gluconeogenic substrate) to allow the return to basal values of the pre-infusion period. The concentrations of the metabolites used in the experiments were based on previous studies.…”

Section: Liver Perfusion Experimentsmentioning

confidence: 99%

Effect of linseed oil and macadamia oil on metabolic changes induced by high‐fat diet in mice

Barrena

Schiavon

Cararra

et al. 2013

The effects of linseed oil (LO) and macadamia oil (MO) on the metabolic changes induced by a high-fat diet (HFD) rich in saturated fatty acid were investigated. For the purpose of this study, the vegetable oil present in the HFD, i.e. soybean oil (SO) was replaced with LO (HFD-LO) or MO (HFD-MO). For comparative purposes, a group was included, which received a normal fat diet (NFD). Male Swiss mice (6-week old) were used. After 14 days under the dietary conditions, the mice were fasted for 18 h, and experiments were then performed. The HFD-SO, HFD-LO and HFD-MO groups showed higher glycaemia (p < 0.05 versus NFD). However, no significant effect was observed on glycaemia, liver gluconeogenesis and liver ketogenesis when SO was replaced by either LO or MO. The body weight and the sum of epididymal, mesenteric, retroperitoneal and inguinal fat weights were higher (p < 0.05) in the HFD-SO and HFD-MO groups as compared with the NFD group. However, there was no significant difference in these parameters between the NFD and HFD-LO groups. Thus, the protective role of LO on lipid accumulation induced by an HFD rich in saturated fatty acid is potentially mediated by the high content of ɷ-3 polyunsaturated fatty acid in LO.

“…Livers were perfused in situ in a non‐recirculating system as previously described . The animals were first anaesthetized with sodium pentobarbital (40 mg kg −1 ) and subjected to laparotomy.…”

Section: Methodsmentioning

confidence: 99%

Instant coffee extract with high chlorogenic acids content inhibits hepatic G‐6‐Pase in vitro, but does not reduce the glycaemia

Bassoli

Cassolla

Borba-Murad

et al. 2015

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Coffee is the main source of chlorogenic acid in the human diet, and it contains several chlorogenic acid isomers, of which the 5-caffeoylquinic acid (5-CQA) is the predominant isomer. Because there are no available data about the action of chlorogenic acids from instant coffee on hepatic glucose-6-phosphatase (G-6-Pase) activity and blood glucose levels, these effects were investigated in rats. The changes on G-6-Pase activity and liver glucose output induced by 5-CQA were also investigated. Instant coffee extract with high chlorogenic acids content (37.8%) inhibited (p < 0.05) the G-6-Pase activity of the hepatocyte microsomal fraction in a dose-dependent way (up to 53), but IV administration of this extract did not change the glycaemia (p > 0.05). Similarly, 5-CQA (1 mM) reduced (p < 0.05) the activity of microsomal G-6-Pase by about 40%, but had no effect (p > 0.05) on glucose output arising from glycogenolysis in liver perfusion. It was concluded that instant coffee extract with high content of chlorogenic acids inhibited hepatic G-6-Pase in vitro, but failed to reduce the glycaemia probably because the coffee chlorogenic acids did not reach enough levels within the hepatocytes to inhibit the G-6-Pase and reduce the liver glucose output.