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1. To examine the role of the hepatic redox state on the rate of gluconeogenesis the effects of sodium crotonate injection (6mmol/kg body wt.) on rat liver metabolite concentrations and gluconeogenesis from lactate were studied in vivo. 2. Crotonate caused a marked oxidation of cytoplasmic and mitochondrial redox couples; decreases were observed in the ratios of [lactate]/[pyruvate], [glycerol 3-phosphate]/[dihydroxyacetone phosphate], [hydroxybutyrate]/[acetoacetate] and measured [NAD+]/[NADH]. 3. Increases occurred in the liver concentrations of all gluconeogenic intermediates from pyruvate through to glucose 6-phosphate, but there was no change in lactate concentration. 4. To determine whether gluconeogenesis from lactate was altered by the more-oxidized hepatic redox state l-[2-14C]lactic acid was infused into the inferior vena cava (50μmol/min per kg body wt.) and the incorporation of radioactivity into blood glucose was measured. 5. Administration of crotonate transiently decreased the rate of lactate incorporation into glucose but within a few minutes the rate of incorporation returned to that of the controls. 6. The results indicate that in these experiments alteration of the NAD+–NADH systems of cytoplasm and mitochondria to a more-oxidized state did not change the rate of gluconeogenesis.

The introduction of the House Sparrow, Passer domesticus, into North America has been a fortuitous natural experiment in avian adaptability. Several attempts have been made to demonstrate morphological variations between various localities resulting from natural selection. The present paper is an examination of some components of the bioenergetics of the House Sparrow with regard to inter-populational differences and their possible adaptive roles. Kendeigh (1934, 1944, and 1949), Seibert (1949) and Davis (1955) have already described existence metabolism and other aspects of the energetics of House Sparrows from central Illinois (latitude 40 °N). In this same area, Barnett (1970) studied mechanisms of seasonal acclimatization, and Zar (1967) experimentally assessed the influence of temperature on lipid composition. Hudson and Kimzey (1966) reported that Houston, Texas, populations had lower standard metabolic rates than those of Michigan, Colorado, and New York.

This paper describes utilization of ingested energy by a population of sand gobies (Gobius minutus) in the Ythan estuary, Scotland, from November 1966 to March 1969. After metamorphosis (July) the gobies survived about 22 months, and their life could be divided into five stages: somatic growth (July–November); gonad growth (November–February); reproduction (February–June); more somatic growth (June–October); and further gonad growth (October–December). I calculated energy budgets for each stage from the relation:[Formula: see text]where: I = ingested calories; M = calories of metabolism; G = calories of growth.Since I had measures of ingestion, growth, and routine oxygen consumption, I hoped to predict active metabolism by the energy ingested not accounted for in growth and routine metabolism. In fact, 0.8I either equalled the sum of growth and routine metabolism or was much too little to explain predicted expenditures for these parameters. Analysis of published feeding and growth studies in fish indicated that energy imbalances of this sort at low rations are general and that fish seem able to shunt more energy into growth when on a restricted ration than one would predict from studies of standard oxygen consumption. This result together with earlier analyses of Paloheimo and Dickie (1966) indicate that energy budgets for natural populations not based on accurate natural ingestion rates are at best only crude approximations.

The subject of the paper is the history of dinitrophenol compounds in relationship to bioenergetics. The history of the interaction between dinitrophenols and bioenergetics can be traced back to 1885 whenCazeneuve andLEpine discovered the thermogenic effects of dinitronapthol. Dinitronapthol and dinitrocresol were used as food colors in the late 19th century although a growing awareness of their toxic properties led to the prohibition of their use for this purpose in certain countries. The toxicity of dinitrophenol was studied in some detail byMayer and his colleagues in France during World War I since it was used by the French in the manufacture of munitions. They recognized that the compound stimulated cellular metabolism, but they did not publish their results until many years later and as a result their work was at first not widely known. In the late 1920's and early 1930's, CorneilleHeymans and his colleagues at Ghent andCutting andTainter and their colleagues at Stanford demonstrated the metabolic stimulating powers of dinitronapthol and dinitrophenol. The Stanford group introduced dinitrophenol into therapeutics for the treatment of obesity, and the drug soon found its way into numerous “anti-fat” patent medicines. Several fatalities, a number of cases of cataract, and other reported toxic effects led to widespread concern about the use of dinitrophenol. The FDA could not take effective action against the drug, however, until after its powers had been expanded by the 1938 Food, Drug and Cosmetic Act. The use of dinitrophenol and related compounds for treating obesity was essentially discontinued after the 1930's. Studies on the mode of action of dinitrophenol in the 1930's and 1940's led ultimately to the establishment of the fact that it uncouples oxidative phosphorylation (Loomis andLipmann, 1948).