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Biomedical subjects

J Mayer

Publications and source records attributed to J Mayer.

At least 307 records · Page 17Linked to original sources
PubMed1978

2-Deoxy-D-glucose induced feeding: relation to diet palatability.

Adult male rats fed either ground Purina Laboratory Chow or the same diet adulterated with 0.5% quinine hydrochloride were tested for feeding in response to the administration of 2-deoxy-D-glucose (2-DG). Three doses of 2-DG were used, 250, 500 and 750 mg/kg of body weight. During a six-hr test period, rats given ground Purina Laboratory Chow ate significantly more following intraperitoneal (IP) injections of 250 and 500 mg/kg of 2-DG than following IP injections of physiological saline. Food intake of animals given Purina Chow also increased after administration of 750 mg/kg of 2-DG but intake was not significantly different from that following saline injections. In contrast to rats maintained on the unadulterated diet, rats given quinine-adulterated chow did not increase intake over saline values during the six-hr test period following administration of 250 and 500 mg/kg of 2-DG, and actually decreased intake after injection of 750 mg/kg of 2-DG. Results are discussed with respect to the role of diet palatability in determining food intake in hungry animals.

Animals↗
PubMed1977

Nutritional outputs and energy inputs in seafoods.

Energy used by U.S. ships in harvesting seafoods can vary by a factor of more than 100 when the seafoods are compared on the basis of their content of edible protein or line weight. This energy difference bears no relationship to the nutritive value in the food. When protein yield is compared, the energy to harvest some seafoods is in the same range as that needed to grow field crops. There is a large increase in energy consumption after processing, partly because of the small percent of the live weight used for human food.

Animals↗
PubMed1977

Energy utilization of a low carbohydrate diet fed genetically obese rats and mice.

Genetically obese Zucker rats, ob/ob mice and non-obese littermates were fed low carbohydrate (2%, 48%, and 50% of energy as carbohydrate, protein, and fat, respectively) and control (60%, 19%, and 21%, as carobhydrate, protein, and fat) diets. The oxidation of the energy components of these diets was measured by adding D-[U-14C]glucose, L-[U-14C]glutamic acid, and glyceryl tri-[1-14C]oleate to test meals given intragastrically and collecting respiratory CO2 for 4 hours. The animals responded to the low carbohydrate diet by oxidizing less glucose and more glutamic acid, but these amounts were proportional to dietary carbohydrate and protein composition, In contrast, the animals oxidized both higher amounts and percentages of glyceryl trioleate when fed the low carbohydrate diet. Obese Zucker rats oxidized less fat than non-obese rats when fed both diets, while obese mice oxidized fat to the same extent as non-obese mice. Feeding the low carbohydrate diet significantly increased body weight in the obese mice, but not in obese rats and non-obese mice and rats. The effect of obesity and the low carbohydrate diet on food intake, serum glucose and lipid values and CO2 production are also reported.

Animals↗
PubMed1977

Changing meal patterns and suppression of feed intake with increasing amounts of dietary nonprotein nitrogen in ruminants.

Goats were injected intraruminally during spontaneous meals with ammonium chloride, urea, ammonium lactate, or sodium lactate arranged in a Latin square experimental design randomized for order of treatments. Urea and ammonium injections shortened meal length by 20 to 30%. Rate of eating and meal frequency were reduced. Sodium lactate injections reduced meal size. In cows, meal length and meal size also were measured. Grain concentrate, corn silage, and chopped hay were fed as complete mixed rations. In the concentrates 58+ of the nitrogen was either from soybean meal or urea. Length of the first meal after feeding was reduced from 24.3 min with soybean meal to 12.4 with urea. Meal size was reduced from 3.2 kg to 1.8 kg when urea was fed. Total feed intake was similar, 12.0 kg/day (soybean meal) and 11.6 kg/day (urea) since spontaneous meal number and size were 17 and .30 kg for soybean meal but increased to 23 and .36 kg for urea. The physiological basis for the limit on meal length with urea rations is unknown but is an important factor in successful feeding of urea when eating time is limited for cows.

Ammonium Chloride↗
PubMed1976

Effects of long-term restricted insulin production in obese-hyperglycemic (genotype ob/ob) mice.

Primary hypersecretion of insulin has been suggested as one possibility for the genetic fault of ob/ob mice. To test this hypothesis, streptozotocin (SZO) was used to reduce permanently insulin secretion in young lean and obese mice. After establishment of hyperglycaemia and weight reduction in treated obese mice (obese-SZO), daily insulin replacment was begun in some (obese-SZO-Ins). Obese-SZO mice maintained insulin levels and body weights similar to lean controls, though they were shorter and fatter, while food intake and blood sugar levels exceeded lean values. Obese-SZO-Ins mice with reduced islet hyperplasia, but great insulin resistance, gained more weight than obese-SZO mice; had high serum insulin and controlled blood glucose; and exhibited hyperphagia. These results suggest that primary hypersecretion of insulin cannot be the genetic defect, as ob/ob mice are hyperphagic, hyperglycaemic, insulin resistant, and "obese" even when insulin levels are restricted.

Animals↗
PubMed1975

Adipose tissue glycerokinase activity in genetic and acquired obesity in rats and mice.

Glycerokinase activity in isolated fat cells was elevated in both Ob/Ob and Db/Db mice in comparison to their lean controls and this elevation was associated with obesity, hyperinsulinemia and hyperglycemia. In the other forms of acquired and genetic obesity in the rats and mice studied (also associated with hyperinsulinemia), adipose tissue glycerokinase activity was not elevated in comparison to lean control groups when expressed on a mg protein basis. It is concluded that the elevated glycerokinase activity is not due to the specific Db or Ob mutation, but is secondary to the obesity and hyperinsulinemia interacting with the similar genetic background in the C57BL/KsJ and the C57BL/6J mouse strains.

Adipose Tissue↗