The effect of protein-deficient isoenergetic diets on the growth of rat jejunal mucosa

Syme, Gabrielle

doi:10.1079/bjn19820084

Cited by 38 publications

(19 citation statements)

References 17 publications

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“…Only later was it realized that fasting could itself produce marked changes in intestinal morphology and function (Levine, Deren, Steiger & Zinno, 1974) and that enterocyte replacement took longer than 24 h to complete (Fry, Lesher, Kisieleski & Sacher, 1963). Isocalorific diets are now used to study sugar effects on enzyme induction Cezard et al 1983) but even this gives no guarantee that crypt cell proliferation will remain constant (Syme, 1982;King, Paterson, Peacock, Smith & Syme, 1983). Using nonmetabolized sugars raises further problems of formulation since this reduces available energy without affecting the gross energy of the diet consumed (Dauncey, 1979).…”

Section: Discussionmentioning

confidence: 99%

Sugar‐dependent selective induction of mouse jejunal disaccharidase activities.

Collins

James

Smith

1989

The Journal of Physiology

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SUMMARY1. Sugar-containing diets chosen not to affect intestinal structure or enterocyte turnover have been fed to mice previously maintained on a low carbohydrate diet in order to determine their ability to induce disaccharidase enzymes in the small intestine.2. Glucose-, fructose-and 3-0-methyl-glucose-containing diets increased sucrase and maltase but not lactase activities in mouse jejunal homogenates. These effects were either absent or negligible in more distal regions of the small intestine.3. Placing mice on glucose-, fructose-or 3-0-methyl-glucose-containing diets was further shown, by quantitative cytochemistry, to cause a 1-6-, 2-6-and 3*2-fold increase in the initial rate at which a-glucosidase activity (sucrase + maltase) appeared in the brush-border membrane of developing enterocytes.4. The time during which a-glucosidase activity increased in enterocyte brushborder membranes fell from 30 h for low carbohydrate fed mice to 21, 19 and 17 h in mice fed glucose, fructose and 3-0-methyl-glucose respectively. Change of diet had no effect on the kinetics of lactase expression by developing enterocytes.5. Maximal a-glucosidase activity detected in enterocyte brush-border membranes is equal to RT, where R is the initial rate of enzyme appearance and T is the time during which this rate operates. The ability of sugars to increase R selectively, but only at the expense of T, defines unexpected limits to the capacity of enterocytes to adapt to changes in luminal nutrition.6. The above results are discussed in relation to other aspects of enterocyte differentiation recently subjected to quantitative analysis. The need to standardize other aspects of intestinal physiology and redefine the energy content of diets containing non-metabolizable substrates in this type of work is also emphasized.

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Section: Discussionmentioning

confidence: 99%

Sugar‐dependent selective induction of mouse jejunal disaccharidase activities.

Collins

James

Smith

1989

The Journal of Physiology

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“…The pelleted semisynthetic experimental diets were made as previously described (25) and contained 5% protein (low-protein diet; LP) or 15% protein (control diet; C) and were generously provided by Dr. R. D. E. Rumsey (Subdepartment of Human Gastrointestinal Physiology and Nutrition, Univ. of Sheffield, Sheffield, UK).…”

Section: Dietsmentioning

confidence: 99%

Persistent Impairment of Insulin Secretory Response to Glucose in Adult Rats After Limited Period of Protein-Calorie Malnutrition Early in Life

1987

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The effect of a limited period of protein-calorie malnutrition in young rats on glucose tolerance, insulin secretory response to glucose, and tissue composition in the adult was studied. Three-week-old rats were weaned onto semisynthetic diets containing either 5% protein (low protein; LP) or 15% protein (control; C) and maintained for 3 wk on their respective diets. At 6 wk of age all rats were returned to a commercial rat chow diet (18% protein). Glucose tolerance, insulin secretory response to glucose, and the protein/DNA ratio in liver, skeletal muscle, heart, kidney, small intestine, and lung were investigated at 3, 6, and 12 wk of age. Rats receiving LP diet failed to gain weight, but growth resumed immediately when they were transferred to commercial rat chow. They did not, however, catch up with C rats. Glucose tolerance and insulin secretory response to glucose remained similar between 3 and 12 wk in C rats. In 6-wk-old LP rats, glucose tolerance was impaired, and the insulin secretory response to glucose was absent. At 12 wk of age the glucose tolerance of the LP rats had normalized, but the insulin secretory response was still blunted. In 6-wk-old LP rats there was an inhibition of the age-dependent increase in cell size, shown by lowered protein/DNA ratios in all tissues studied. This decrease in cell size persisted at 12 wk in liver, skeletal muscle, heart, and lung. We conclude that protein-calorie malnutrition early in life persistently impairs the insulin secretion. The persistently lowered protein/DNA ratios in many tissues may be related to this lowered capacity for insulin secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…Values are means for six rats in each experimental composition see Refs. Syme, 1982, andSwenne et al, 1987). Diets were group.…”

Section: Animals and Dietsmentioning

confidence: 99%

Cyanide Detoxification in Rats Exposed to Acetonitrile and Fed a Low Protein Diet

Swenne¹

1996

Fundamental and Applied Toxicology

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Different neurological syndromes have been associated with exposure to cyanide. Dietary cyanide exposure from cassava roots combined with a low intake of the sulfur amino acids necessary for cyanide detoxification has been implicated in the causation of konzo, an upper motoneuron disease identified in Africa. We have investigated the effect of a low protein diet on the capacity for cyanide detoxification. Rats were fed normal chow containing 18% protein or a low protein diet with 5% protein. To expose rats to cyanide the drinking water was supplemented with 40 or 80 mM acetonitrile (CH3CN) for up to 4 weeks. Weight gain was monitored and 24-hr urines were collected for analyses of total sulfur, inorganic sulfate, thiocyanate, and 2-aminothiolazine-4-carboxylic acid (ATC). Blood was collected for analyses of cyanide and cyanate. Rats on a normal diet grew throughout the experiment, while those on a low protein diet initially lost weight and then stabilized at a constant weight. Rats exposed to acetonitrile all progressively lost weight, those on a low protein diet at the highest rate. Signs of neurological damage were not observed. Rats not exposed to acetonitrile excreted < 0.2% of sulfur as thiocyanate and those on a low protein diet reduced their total sulfur excretion to one-third that of rats of the normal diet. Rats on the normal diet did not change total sulfur excretion during exposure to acetonitrile, although thiocyanate now contributed more than two-thirds of excreted sulfur. Rats on a low protein diet exposed to acetonitrile increased both total sulfur and thiocyanate excretion to the levels of rats on a normal diet. Rats exposed to acetonitrile had manyfold increases of circulating concentrations of cyanide and cyanate and of urinary excretion of ATC. There was a positive correlation between blood cyanide concentrations and the plasma concentration of cyanate. It is concluded that the rat has a high capacity for detoxification of cyanide. During adaptation to a low protein intake, sulfur is conserved but cyanide detoxification is still possible at the cost of extensive protein catabolism. It is thus possible that subclinical cyanide exposure could interfere with normal growth and development. The observation of a relationship between circulating cyanide on the one hand and circulating cyanate and urinary excretion of ATC on the other highlights the possibility that cyanide metabolites may mediate neurotoxic effects of cyanide.

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The effect of protein-deficient isoenergetic diets on the growth of rat jejunal mucosa

Cited by 38 publications

References 17 publications

Sugar‐dependent selective induction of mouse jejunal disaccharidase activities.

Sugar‐dependent selective induction of mouse jejunal disaccharidase activities.

Persistent Impairment of Insulin Secretory Response to Glucose in Adult Rats After Limited Period of Protein-Calorie Malnutrition Early in Life

Cyanide Detoxification in Rats Exposed to Acetonitrile and Fed a Low Protein Diet

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