Nutritional and Metabolic Characterization of a Thiamine‐Deficient Rat Model

The "Cayuga syndrome" is a maternally transmitted, naturally occurring thiamine deficiency that causes 100% mortality of larval landlocked Atlantic salmon Salmo salar in several of New York's Finger Lakes . Results of multiyear studies to qualify and quantify the neurobehavioral and gross pathological signs of this condition are described . Affected sac fry became weak and ataxic and responded atypically to stimuli 1-2 weeks before death . Quantitative assays of stimulus-provoked swimming revealed a significant neuropathy whereby the sac fry exhibited abnormal thigmotactic and phototactic behaviors . Gross lesions observed in Cayuga sac fry included yolk-sac opacities, subcutaneous edema, vitelline hemorrhage or congestion, pericardial edema, retrobulbar edema, branchial congestion, foreshortened maxillae, hydrocephalus, and occasional caudal fin deformities. Lesion frequency in progeny differed significantly between dam source . Yolk conversion efficiency was decreased at least 1 week before death, suggesting that the bioenergetics of the fish was compromised and thereby supporting the thiamine residue and treatment data reported elsewhere . Comparisons with coagulated-yolk, blue-sac and swim-up syndromes are presented . The pathological signs of the Cayuga syndrome represent a unique departure from the lesions induced by toxicants or pathogens in other piscine models, and for the first time profile the profound effects of thiamine deficiency on cardiovascular and neurological systems of larval fish .Nielson 1959) . Coagulated-yolk has been attributed to bacterial infection (Von Betegh 1912 ; Guberlet et al . 1931), rough handling (Dietrich 1939 ; I Address reprint requests to

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Section: Discussionmentioning

confidence: 99%

Pathological and Behavioral Manifestations of the “Cayuga Syndrome,” a Thiamine Deficiency in Larval Landlocked Atlantic Salmon

Fisher

Spitsbergen

Iamonte

et al. 1995

Journal of Aquatic Animal Health

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“…Thiamine deficiency causes acidosis resulting from increased plasma concentrations of pyruvate and lactate (Combs 1992). These alpha-keto acids accumulate because of the inhibition of thiamine pyrophosphate-dependent pyruvate dehydrogenase (enzyme code 1.2.4.1) action (Molina et al 1994). Egg thiamine levels in Salmon River Chinook Salmon are also suggestive of thiamine-linked impairment of migration; levels were lower in salmon collected from the lower Salmon River relative to the upper Salmon River in 2015-2017 .…”

Section: Discussionmentioning

confidence: 99%

Ontogenetic Dietary Changes and Thiamine Status of Lake Ontario Chinook Salmon, 2005–2006

Fitzsimons

Honeyfield

Rush

2021

N American J Fish Manag

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In the Great Lakes, an Alewife Alosa pseudoharengus diet has been reported to cause thiamine deficiency in salmonines as a result of high thiaminase activity. The ontogeny of thiamine deficiency and its relationship to Alewife consumption have not been determined in Chinook Salmon Oncorhynchus tshawytscha within this system. Using stable isotope mixing models along with muscle thiamine, we assessed ontogenetic changes in the diet and corresponding muscle thiamine status of Lake Ontario Chinook Salmon ranging in TL from 100 to 1,000 mm. Thiamine levels were highest in young of the year collected in a tributary of Lake Ontario but declined once Chinook Salmon entered Lake Ontario. In Lake Ontario, the diets of juvenile (200-400 mm; 97-99%) and adult (>400 mm; 97-100%) Chinook Salmon consisted almost entirely of Alewives as estimated using mixing models. This Alewife diet was associated with an ontogenetic decline in muscle thiamine among Chinook Salmon. The asymptotic decline in thiamine concentration with increasing size plateaued at 720-758 pmol/g of muscle. The proportion of individuals below a thiamine threshold of 500 pmol/g (associated with a loss of equilibrium) increased with TL up to 799 mm and then declined between 800 and 1,000 mm. At these muscle concentrations, no outward signs of thiamine deficiency were observed. Calculation of total mass accumulation of body stores of thiamine (muscle concentration times body weight) showed an unexpected and significant increase with size. Although it appears that dietary Alewives affected thiamine status, there were undetermined factors, such as incomplete destruction of thiamine by thiaminase, gut synthesis of thiamine, gill absorption of water thiamine, and/or other factors, that contributed to the overall thiamine status of these Chinook Salmon.Chinook Salmon Oncorhynchus tshawytscha were intentionally stocked in the Great Lakes beginning in the 1960s to control the overabundant populations of nonindigenous Alewives Alosa pseudoharengus and to create a recreational sport fishery (Tanner 1971). Alewives, which have a high thiaminase (enzyme code 2.5.1.2; IUBMB 1992) activity (Tillitt et al. 2005), are found throughout the Great Lakes basin, where they comprise a major proportion of the diet of salmonines, including Chinook Salmon, Coho Salmon Oncorhynchus kisutch, and Lake Trout Salvelinus

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“…In control animals, this decrease was 14% of initial level (C 0 vs. C 30 ). Prolonged deprivation of dietary thiamine (6 weeks) resulted in rats in significant decreased serum insulin up to 37% (Molina et al, 1994).…”

Section: Discussionmentioning

confidence: 99%

“…These meals cause a lowering of blood lipids concentrations in humans (Brighenti et al, 1999;Letexier et al, 2003). Thiamine deficiency resulted in almost a twofold increase of lactate concentration (Pannunzio et al, 2000) and 20% loss of activity of pyruvate decarboxylase (Molina et al, 1994) as well as a-ketoglutarate dehydrogenase (Blair et al, 1999). Additionally, vitamin B 1 deficiency may be a reason of accumulation of reduced NADH + H + , and FADH 2 , and acidic intermediates of glycolysis-pyruvic and lactic acids (Molina et al, 1994;Pannunzio et al, 2000;Ham and Karska-Wysocki, 2005).…”

Section: Discussionmentioning

confidence: 99%

“…Thiamine deficiency resulted in almost a twofold increase of lactate concentration (Pannunzio et al, 2000) and 20% loss of activity of pyruvate decarboxylase (Molina et al, 1994) as well as a-ketoglutarate dehydrogenase (Blair et al, 1999). Additionally, vitamin B 1 deficiency may be a reason of accumulation of reduced NADH + H + , and FADH 2 , and acidic intermediates of glycolysis-pyruvic and lactic acids (Molina et al, 1994;Pannunzio et al, 2000;Ham and Karska-Wysocki, 2005). Inhibition of oxidative processes in glycolysis and Krebs' cycle accompanied by accumulation of reduced transporters of hydrogen ions is the reason of suppression of ATP synthesis in oxidative phosphorylation process.…”

Section: Discussionmentioning

confidence: 99%

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Effect of inulin and oligofructose enrichment of the diet on rats suffering thiamine deficiency

Debski

Kuryl

Gralak

et al. 2010

Journal of Animal Physiology and Animal Nutrition

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Thiamine deficiency resulted in inhibition of two main pathways supplying energy to the tissues: glycolysis and β-oxidation. Glycolysis was found to be inhibited to 40% of initial value calculated on the basis of RBC trans-membrane transport of glucose. Prolongation of experiment cause lowering of uptake of this sugar. In rats, energy production from fatty acids (FA) seems to be less sensitive to thiamine deficiency than glycolysis. After 30 days of feeding, utilization of FA in rats was depressed to the 61% of initial value. Thiamine deficiency suppressed insulin secretion, and the changes were statistically significant. Feeding of rats with thiamine restricted diet for 1 month caused the reduction of serum insulin by 14%. In the same animals, trans-membrane glucose transport was reduced over two-times, what might suggest a decreased efficiency of insulin action in such conditions. The kind and concentration of non-digestible fructo-oligosaccharides (FOS) did not affect significantly serum insulin concentration in animals fed thiamine restricted diet. Substitution of a part of wheat starch with FOS has only insignificant compensatory effect on the uptake of glucose. A partial amelioration of the β-oxidation inhibition caused by feeding rats with thiamine deficient diet was observed in animals supplemented with FOS. However, this effect was statistically significant only in rats receiving diet containing 10% of inulin. The effect of supplemented FOS and their concentration on trans-membrane glucose transport in RBC was statistically significant, when pulled supplementation groups were used for statistical evaluation.

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Nutritional and Metabolic Characterization of a Thiamine‐Deficient Rat Model

Cited by 16 publications

References 16 publications

Pathological and Behavioral Manifestations of the “Cayuga Syndrome,” a Thiamine Deficiency in Larval Landlocked Atlantic Salmon

Pathological and Behavioral Manifestations of the “Cayuga Syndrome,” a Thiamine Deficiency in Larval Landlocked Atlantic Salmon

Ontogenetic Dietary Changes and Thiamine Status of Lake Ontario Chinook Salmon, 2005–2006

Effect of inulin and oligofructose enrichment of the diet on rats suffering thiamine deficiency

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