Change of blood sugar and plasma insulin levels of fishes in glucose tolerance test.

108

SUMMARYRainbow trout have a limited ability to use dietary carbohydrates efficiently and are considered to be glucose intolerant. Administration of carbohydrates results in persistent hyperglycemia and impairs post-prandial down regulation of gluconeogenesis despite normal insulin secretion. Since gluconeogenic genes are mainly under insulin control, we put forward the hypothesis that the transcriptional function of insulin as a whole may be impaired in the trout liver. In order to test this hypothesis, we performed intraperitoneal administration of bovine insulin to fasted rainbow trout and also subjected rainbow trout primary hepatocytes to insulin and/or glucose stimulation. We demonstrate that insulin was able to activate Akt, a key element in the insulin signaling pathway, and to regulate hepatic metabolism-related target genes both in vivo and in vitro. In the same way as in mammals, insulin decreased mRNA expression of gluconeogenic genes, including glucose 6-phosphatase (G6Pase), fructose 1,6-bisphosphatase (FBPase) and phosphoenolpyruvate carboxykinase (PEPCK). Insulin also limited the expression of carnitine palmitoyltransferase 1 (CPT1), a limiting enzyme of fatty acid β-oxidation. In vitro studies revealed that, as in mammals, glucose is an important regulator of some insulin target genes such as the glycolytic enzyme pyruvate kinase (PK) and the lipogenic enzyme fatty acid synthase (FAS). Interestingly, glucose also stimulates expression of glucokinase (GK), which has no equivalent in mammals. This study demonstrates that insulin possesses the intrinsic ability to regulate hepatic gene expression in rainbow trout, suggesting that other hormonal or metabolic factors may counteract some of the post-prandial actions of insulin.

Section: Introductionmentioning

confidence: 99%

Insulin regulates the expression of several metabolism-related genes in the liver and primary hepatocytes of rainbow trout (Oncorhynchus mykiss)

Plagnes-Juan

Lansard

Seiliez

et al. 2008

108

“…Although initially the basis for this poor metabolic glucose utilization was though to be a deficiency in insulin secretion (Furuichi and Yone, 1981;Palmer and Ryman, 1972), later hormone titration in several fish species demonstrated that plasma insulin levels in piscine species are even higher than in mammals (Mommsen and Plisetskaya, 1991). The secretagogues of insulin in fish are the same as in mammals, and although glucose is not the most potent of these, generally hyperglycaemia does result in hyperinsulinaemia (Moon, 2001).…”

Section: Introductionmentioning

confidence: 99%

Insulin-induced hypoglycaemia is co-ordinately regulated by liver and muscle during acute and chronic insulin stimulation in rainbow trout (Oncorhynchus mykiss)

Polakof

Skiba‐Cassy

Choubert

et al. 2010

SUMMARYThe relative glucose intolerance of carnivorous fish species is often proposed to be a result of poor peripheral insulin action or possibly insulin resistance. In the present study, data from aortic cannulated rainbow trout receiving bovine insulin (75 mIU kg -1 ) injections show for the first time their ability to clear glucose in a very efficient manner. In another set of experiments, mRNA transcripts and protein phosphorylation status of proteins controlling glycaemia and glucose-related metabolism were studied during both acute and chronic treatment with bovine insulin. Our results show that fasted rainbow trout are well adapted at the molecular level to respond to increases in circulating insulin levels, and that this hormone is able to potentially improve glucose distribution and uptake by peripheral tissues. After acute insulin administration we found that to counter-regulate the insulininduced hypoglycaemia, trout metabolism is strongly modified. This short-term, efficient response to hypoglycaemia includes a rapid, coordinated response involving the reorganization of muscle and liver metabolism. During chronic insulin treatment some of the functions traditionally attributed to insulin actions in mammals were observed, including increased mRNA levels of glucose transporters and glycogen storage (primarily in the muscle) as well as decreased mRNA levels of enzymes involved in de novo glucose production (in the liver). Finally, we show that the rainbow trout demonstrates most of the classic metabolic adjustments employed by mammals to efficiently utilize glucose in the appropriate insulin context.

“…Glucose-only infusion Glucose-only infusion (Bucking and Wood, 2004) Glucose and phlorizin infusion Despite the fact that most fish are considered to behave as diabetic-like animals, experiencing prolonged hyperglycemia after ingesting a carbohydrate-rich meal (Palmer and Ryan, 1972;Furuichi and Yone, 1981;Wilson, 1994;Wright et al, 1998), in vivo renal handling of glucose by fish has rarely been examined directly. Carbohydrates found in fish feed are generally various forms of starches obtained from grains, such as corn or wheat (Horn, 1998).…”

mentioning

confidence: 99%

Renal regulation of plasma glucose in the freshwater rainbow trout

Bucking

Wood

2005

SUMMARY This study examined the effects of prolonged hyperglycemia on renal handling of glucose and explored the in vivo pharmacological effects of phlorizin on glucose transport in the rainbow trout. The transport of glucose was examined by experimentally elevating the rate of renal glucose reabsorption via infusion of the fish with exogenous glucose at a rate of 70 μmol kg–1 h–1 and by inactivating the glucose transporters via the simultaneous administration of phlorizin (1 μmol kg–1h–1). Glucose was reabsorbed against a concentration gradient, until plasma glucose levels reached ∼22 μmol l–1 and the transport maximum of glucose in the kidney(∼145 μmol kg–1 h–1) was exceeded. At this point, glucose was lost to the urine, resulting in glucosuria. Glucosuria affected water reabsorption, approximately doubling the water clearance ratio,and resulted in osmotic diuresis. This in turn reduced Na+reabsorption, increasing the amount lost to the urine from 0.5% to 2% of the filtered load. Glucose reabsorption was found to be correlated with Na+ reabsorption, though the latter was almost 10-fold higher than glucose transport rates. Phlorizin treatment reduced glucose reabsorption,although it did not block it entirely until 48–72 h of infusion. The glucosuria resulting from the blockade of the glucose transporters resulted in a similar osmotic diuresis and a greater Na+ loss to the urine (9%of filtered load). The results are discussed with respect to the net renal`wasting' of glucose and the detrimental osmoregulatory and ionoregulatory effects associated with glucosuria caused by carbohydrate-rich diets.