Responses of the perfused liver of neonatal type 2 diabetic rats to gluconeogenic and ammoniogenic substrates

Carvalho-Martini, Mirian; Suzuki‐Kemmelmeier, Fumie; Oliveira, Denise Silva de; Comar, Jurandir Fernando; Bracht, Adelar

doi:10.4236/health.2010.25071

Cited by 2 publications

(3 citation statements)

References 29 publications

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“…On the other hand, there is also a report of diminished rates of gluconeogenesis from lactate in perfused livers from alloxan diabetic rats [ 45 ]. Similar results were obtained in the perfused liver of type 2 diabetic rats where gluconeogenesis from lactate, alanine and glycerol was clearly diminished [ 24 ]. The high basal rates of glycogenolysis due to the high glycogen levels and the way by which the gluconeogenic activity was calculated from the total rates of glucose release could have contributed to these different reports.…”

Section: Discussionsupporting

confidence: 84%

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The Metabolic Responses to L-Glutamine of Livers from Rats with Diabetes Types 1 and 2

et al. 2016

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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 β-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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Section: Discussionsupporting

confidence: 84%

“…Neonatal type 2 diabetes mellitus was induced as described previously [ 23 , 24 ]. Male newborn (2 days old) Wistar rats were injected intraperitoneally with streptozotocin (150 mg/kg) dissolved in citrate buffer (10 mM; pH 4.5).…”

Section: Methodsmentioning

confidence: 99%

The Metabolic Responses to L-Glutamine of Livers from Rats with Diabetes Types 1 and 2

et al. 2016

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“…It should be mentioned that elevated plasma levels of this hormone have been found in obese, prediabetic, and type 2 diabetic conditions [ 20 , 64 , 65 ]. In the isolated perfused rat liver, the gluconeogenesis rate relies on the liver enzymatic capacity, which reflects the medium- and long-term effects of the circulating hormones (e.g., insulin/glucagon ratio in the portal vein) [ 66 ]. Therefore, an upregulation of genes coding for gluconeogenic enzymes such as fructose-1,6-biphosphatase is a real possibility in CAF rat livers.…”

Section: Discussionmentioning

confidence: 99%

Cafeteria Diet Feeding in Young Rats Leads to Hepatic Steatosis and Increased Gluconeogenesis under Fatty Acids and Glucagon Influence

et al. 2018

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Gluconeogenesis overstimulation due to hepatic insulin resistance is the best-known mechanism behind elevated glycemia in obese subjects with hepatic steatosis. This suggests that glucose production in fatty livers may differ from that of healthy livers, also in response to other gluconeogenic determinant factors, such as the type of substrate and modulators. Thus, the aim of this study was to investigate the effects of these factors on hepatic gluconeogenesis in cafeteria diet-induced obese adult rats submitted to a cafeteria diet at a young age. The livers of the cafeteria group exhibited higher gluconeogenesis rates when glycerol was the substrate, but lower rates were found when lactate and pyruvate were the substrates. Stearate or glucagon caused higher stimulations in gluconeogenesis in cafeteria group livers, irrespective of the gluconeogenic substrates. An increased mitochondrial NADH/NAD+ ratio and a reduced rate of 14CO2 production from [14C] fatty acids suggested restriction of the citric acid cycle. The higher glycogen and lipid levels were possibly the cause for the reduced cellular and vascular spaces found in cafeteria group livers, likely contributing to oxygen consumption restriction. In conclusion, specific substrates and gluconeogenic modulators contribute to a higher stimulation of gluconeogenesis in livers from the cafeteria group.

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Responses of the perfused liver of neonatal type 2 diabetic rats to gluconeogenic and ammoniogenic substrates

Cited by 2 publications

References 29 publications

The Metabolic Responses to L-Glutamine of Livers from Rats with Diabetes Types 1 and 2

The Metabolic Responses to L-Glutamine of Livers from Rats with Diabetes Types 1 and 2

Cafeteria Diet Feeding in Young Rats Leads to Hepatic Steatosis and Increased Gluconeogenesis under Fatty Acids and Glucagon Influence

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