Control of glycogen deposition

Ferrer, Juan C.; Favre, Cristián; Gomis, Roger R.; Fernández‐Novell, Josep M.; Garcı́a-Rocha, Mar; Iglesia, Núria de la; Cid, Emili; Guinovart, Joan J.

doi:10.1016/s0014-5793(03)00565-9

Cited by 187 publications

(167 citation statements)

References 54 publications

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“…Indeed, G6P not only constitutes the crossroads of several metabolic pathways but also plays a key role as a signal molecule in regulating hepatic glucose and glycogen metabolism. An increase in G6P levels induces the activation of GS through cellular redistribution of the enzyme and activation of the phosphatase 1 proteins that mediate GS dephosphorylation (19). Moreover, exogenous glucose and gluconeogenesis are equally effective in increasing intracellular G6P (33) and activating GS (23).…”

Section: Discussionmentioning

confidence: 99%

Liver glyconeogenesis: a pathway to cope with postprandial amino acid excess in high-protein fed rats?

Azzout‐Marniche¹,

Gaudichon²,

Blouet³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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This paper provides molecular evidence for a liver glyconeogenic pathway, that is, a concomitant activation of hepatic gluconeogenesis and glycogenesis, which could participate in the mechanisms that cope with amino acid excess in high-protein (HP) fed rats. This evidence is based on the concomitant upregulation of phosphoenolpyruvate carboxykinase (PEPCK) gene expression, downregulation of glucose 6-phosphatase catalytic subunit (G6PC1) gene expression, an absence of glucose release from isolated hepatocytes and restored hepatic glycogen stores in the fed state in HP fed rats. These effects are mainly due to the ability of high physiological concentrations of portal blood amino acids to counteract glucagon-induced liver G6PC1 but not PEPCK gene expression. These results agree with the idea that the metabolic pathway involved in glycogen synthesis is dependent upon the pattern of nutrient availability. This nonoxidative glyconeogenic disposal pathway of gluconeogenic substrates copes with amino excess and participates in adjusting both amino acid and glucose homeostasis. In addition, the pattern of PEPCK and G6PC1 gene expression provides evidence that neither the kidney nor the small intestine participated in gluconeogenic glucose production under our experimental conditions. Moreover, the main glucose-6-phosphatase (G6Pase) isoform expressed in the small intestine is the ubiquitous isoform of G6Pase (G6PC3) rather than the G6PC1 isoform expressed in gluconeogenic organs.high-protein diet; glyconeogenesis; glucose 6-phosphatase; phosphoenolpyruvate carboxykinase; liver THE CONSEQUENCES OF HIGH-PROTEIN feeding on the regulation and pathways of glucose disposal through glycogen metabolism and gluconeogenesis remain unclear. High-protein feeding induced both insulin and glucagon secretion in the fed state, associated with the repletion of glycogen stores (3, 45, 52), whereas excess dietary amino acids are metabolized within tissues and the derived nitrogen released into the circulation in the form of glutamine, alanine, serine, and glycine (28, 56). These amino acids are subsequently taken up by the liver, and the nitrogen is converted to urea and glutamine (12,28), the bulk of their carbon skeleton being converted to glucose through hepatic gluconeogenesis (8,29,37,51). This concomitant activation of both glycogen synthesis and gluconeogenesis in the fed state raises the question as to whether the glucose-6-P produced from gluconeogenic amino acid precursors could be directly channeled to glycogen through glycogenesis instead of being excreted as glucose from hepatocytes. This pathway of glyconeogenesis has been discussed over several decades, but despite some evidence during refeeding (49), its significance and molecular basis remain poorly understood (4, 30), and it has not previously been hypothesized under high-protein feeding.It is established that insulin stimulates glycogen synthesis and represses the gluconeogenic production of glucose, whereas glucagon represses glycogen synthesis and stimulates glucose ...

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Section: Discussionmentioning

confidence: 99%

Liver glyconeogenesis: a pathway to cope with postprandial amino acid excess in high-protein fed rats?

Azzout‐Marniche¹,

Gaudichon²,

Blouet³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Particularly important is the fact that dietary amino acids and sugars differentially control the relative amounts of insulin and glucagon to be secreted by the pancreas (Young, 2005;Ji and Bachmanov, 2007), an effect that will directly influence the organism's ability to mobilize stored fuels (Ferrer et al, 2003;Buch et al, 2008). This suggests that appetites for these macronutrients might be under the control of metabolic needs in addition to taste quality, as evidenced by increased intake levels of essential amino acids that had been withdrawn from an animal's diet (Markison et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

Nutrient Selection in the Absence of Taste Receptor Signaling

Ren¹,

Ferreira²,

Zhou³

et al. 2010

Journal of Neuroscience

141

161

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When allowed to choose between different macronutrients, most animals display a strong attraction toward carbohydrates compared with proteins. It remains uncertain, however, whether this food selection pattern depends primarily on the sensory properties intrinsic to each nutrient or, alternatively, metabolic signals can act independently of the hedonic value of sweetness to stimulate elevated sugar intake. Here we show that Trpm5 Ϫ/Ϫ mice, which lack the cellular mechanisms required for sweet and several forms of L-amino acid taste transduction, develop a robust preference for D-glucose compared with isocaloric L-serine independently of the perception of sweetness. Moreover, a close relationship was found between glucose oxidation and taste-independent nutrient intake levels, with animals increasing intake as a function of glucose oxidation rates. Furthermore, microdialysis measurements revealed nutrient-specific dopaminergic responses in accumbens and dorsal striatum during intragastric infusions of glucose or serine. Specifically, intragastric infusions of glucose induced significantly higher levels of dopamine release compared with isocaloric serine in both ventral and dorsal striatum. Intragastric stimulation of dopamine release seemed to depend on glucose utilization, because administration of an anti-metabolic glucose analog resulted in lower dopamine levels in striatum, an effect that was reversed by intravenous glucose infusions. Together, our findings suggest that carbohydrate-specific preferences can develop independently of taste quality or caloric load, an effect associated with the ability of a given nutrient to regulate glucose metabolism and stimulate brain dopamine centers.

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“…Insulin is a hormone produced by β-cells in the pancreas after exposure to hyperglycemic conditions, and then acts to trigger tissues in the body to absorb glucose from the blood. A lack of insulin in the case of diabetes leads to severe dysfunction in the target organs as muscle, liver and adipose tissue (1,2). The mechanisms of glucose-dependent insulin secretion have been examined by applying β-cells blockers (3).…”

Section: Introductionmentioning

confidence: 99%

Polysaccharide isolated from Triticum aestivum stimulates insulin release from pancreatic cells via the ATP-sensitive K+ channel

et al. 2012

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Abstract. Traditional natural plants have been used throughout the world for their antidiabetic effects. The aim of the present study was to investigate the stimulating activity of a polysaccharide extract derived from T. aestivum sprout (TASP) on insulin secretion in vitro using the RIN-5F pancreatic β-cell line and rat pancreatic islets. In these experiments, TASP (0.1 to 2 mg/ml) augmented glucose-stimulated insulin secretion in a dose-dependent manner in the presence of a stimulatory glucose concentration (16.7 mM), but not of a basal concentration (1.1 mM). Although TASP failed to enhance the high K + -induced insulin secretion, the insulinotropic effect of TASP was significantly inhibited by diazoxide, an opener of ATP-sensitive K + channel blocking insulin release. TASP potentiated the insulin secretion induced by other secretagogues, such as IBMX and tolbutamide. Moreover, glucose-derived blood insulin levels were significantly elevated by oral administration of TASP to mice, similarly to antidiabetic drugs. We also demonstrated that TASP significantly increased glucose-induced 45 Ca2+ uptake and proinsulin mRNA expression in rat islets. Overall, our results suggest that TASP has a stimulating effect on insulin secretion and production in pancreatic β-cells via K + channel closure and calcium influx. These results suggest that TASP may be useful as a candidate for the therapy of diabetes mellitus.

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Control of glycogen deposition

Cited by 187 publications

References 54 publications

Liver glyconeogenesis: a pathway to cope with postprandial amino acid excess in high-protein fed rats?

Liver glyconeogenesis: a pathway to cope with postprandial amino acid excess in high-protein fed rats?

Nutrient Selection in the Absence of Taste Receptor Signaling

Polysaccharide isolated from Triticum aestivum stimulates insulin release from pancreatic cells via the ATP-sensitive K+ channel

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