Renal Function in the Choline Deficient Rat

Michael, U. F.; Cookson, S. L.; Chavez, Rafaelita; Pardo, Victoriano

doi:10.3181/00379727-150-39103

Cited by 20 publications

(5 citation statements)

References 10 publications

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“…Another grouping of metabolites ( myo ‐inositol, CMPF, hippurate, and 3‐indolepropionate) that changed in choline deficiency is related to renal function. In animals, choline deficiency is associated with a defect in reabsorption of water in the renal distal tubule (55), and it is possible that concentrations of these metabolites are lower in choline deficiency because they are being lost with excess water in urine. Myo ‐inositol, like betaine, is one of the major organic osmolytes used frequently by mammalian cells to regulate volume in response to hypertonic stress (56, 57).…”

Section: Discussionmentioning

confidence: 99%

Metabolomic profiling can predict which humans will develop liver dysfunction when deprived of dietary choline

et al. 2010

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Choline is an essential nutrient, and deficiency causes liver and muscle dysfunction. Common genetic variations alter the risk of developing organ dysfunction when choline deficient, probably by causing metabolic inefficiencies that should be detectable even while ingesting a normal choline-adequate diet. We determined whether metabolomic profiling of plasma at baseline could predict whether humans will develop liver dysfunction when deprived of dietary choline. Fifty-three participants were fed a diet containing 550 mg choline/70 kg/d for 10 d and then fed < 50 mg choline/70 kg/d for up to 42 d. Participants who developed organ dysfunction on this diet were repleted with a choline-adequate diet for > or = 3 d. Plasma samples, obtained at baseline, end of depletion, and end of repletion, were used for targeted and nontargeted metabolomic profiling. Liver fat was assessed using magnetic resonance spectroscopy. Metabolomic profiling and targeted biochemical analyses were highly correlated for the analytes assessed by both procedures. In addition, we report relative concentration changes of other small molecules detected by the nontargeted metabolomic analysis after choline depletion. Finally, we show that metabolomic profiles of participants when they were consuming a control baseline diet could predict whether they would develop liver dysfunction when deprived of dietary choline.

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Section: Discussionmentioning

confidence: 99%

Metabolomic profiling can predict which humans will develop liver dysfunction when deprived of dietary choline

et al. 2010

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“…For example, extracellular fluid increase restrains the renin secre tion (in the same way as aldosterone) and the formation of edema acts against hypervolemia [Fournier and Lagrue, 1971], We will add thyroxin and diet to the factors which modulate the response. In this way, a hypo thyroid state and a diet poor in protein and Na ensure some protection from the occurrence of hypertension [Berg and Sims, 1965], On the other hand, a lack of B factors and a diet with a glucidic excess promote hypertension [Hackel et al, 1965;Michael et al, 1975],…”

Section: Resultsmentioning

confidence: 99%

Stress-effects in Microcebus murinus

Perret¹

1982

IJFP

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Histological investigations were made over a 10-year period on 164 lesser mouse lemurs that died spontaneously in captivity. The principal lesions found were chronic nephrosis with nephritis which affects 90% of the animals, myocardial necrosis, respiratory insufficiency induced by interstitial pneumonia, fatty changes in the liver, and splenic and gastric lesions. The following are associated with these pathologies: progressive hypothyroidism, stable hypercorticism, slight medulloadrenal hyperactivity, and sexual disorders such as testicular atrophy in males and estrous cycle disturbance or uterine tumor in females. All these data were treated by correspondence analysis; this showed that, except for some rare cases of death which can be attributed to massive parasitic infestation or generalized cancer, the whole captive population of lesser mouse lemurs is suffering from a syndrome that leads to renal insufficiency and death. Most of the observed pathologies are considered as being associated with aging in mammals. But captive Microcebus murinus died between 3 and 4 years of age, whereas their potential life survival is 13 years. Our hypothesis is that these pathologies arise due to an overload of cortico- and medulloadrenal secretions. The above-mentioned hormonal imbalance could be induced by stress factors occurring in captivity, the most important of which would be social stress.

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“…Choline deficiency is known to compromise renal functions and cause kidney toxicity in laboratory animals (Baxter, 1947;Michael et al, 1975;Zeisel and Blusztajn, 1994).…”

Section: Discussionmentioning

confidence: 99%