Published Science

Extant terrestrial mammals span an enormous size range, from tiny pygmy shrews weighing in at less than 5 g to massive African elephants tipping the scales at over 2500 kg (Eisenberg, 1981). Despite such marked differences in adult body mass, Alexander et al. (1979) report that the lengths and diameters of limb bones in a shrew-to-elephant size series scale surprisingly close to geometric similarity; i.e., linear dimensions are almost proportional to (mass)173. Although adult members of the order Primates cannot match the overall range of body sizes in mammals, the size distribution of living primate species is still quite impressive, ranging from dwarf galagos and mouse lemurs (—60–70 g) at one end of the spectrum to male gorillas (>200 kg in some individuals) at the other. Given the unexpected results of the Alexander et al. (1979) study, it is reasonable to wonder if the linear dimensions of the long bones of adult primates also conform to the expectations of geometric similarity. A few minutes of casual observation at the zoo or natural history museum would probably suffice to allow one to reject this null hypothesis for primate limb proportions. Galagos and tarsiers simply do not resemble gibbons or gorillas very much with regard to their respective bodily proportions. Locomotor differences between these extremes seem equally obvious and appear to be correlated with differences in limb proportions.

Interspecific allometric analysis rests upon the assumption that individual characteristics typically change in a regular, predictable fashion with body size according to some recognizable scaling principle, unless special adaptation has led to fundamental reorganization identifiable as a grade shift (see Martin, 1980).

The effect on lipoprotein metabolism of a 2-week modified fast and an immediately ensuing 3-week period on a vegetarian diet was studied under metabolic ward conditions in 21 non-obese female and 6 male patients. The very low calorie diet induced reductions of the cholesterol concentration in all serum lipoprotein classes. In the female patients, who were all normolipoproteinaemic, the triglycerides in serum showed a slight increase during the fast, reflecting small changes in very low (VLDL) and low density lipoprotein triglycerides. This may probably be explained partly by simultaneous significant reductions of both the adipose tissue and skeletal muscle tissue lipoprotein lipase activities (LPLA). In contrast, in the male patients who had a higher VLDL level at admission, the VLDL triglycerides decreased without significant changes of high density lipoprotein (HDL) cholesterol and of LPLA in muscle. The female patients, whose weights were stable during the vegetarian diet, ended up with a lower HDL cholesterol than at the start of the trial. This effect was probably partly due to the high content of polyunsaturated fatty acids in the vegetarian diet. It is concluded that the changes of lipoprotein metabolism during supplemented fasting are quantitatively and qualitatively different in several respects in females and males.

There is no doubt that the primates are a highly diverse and specialized order of animals: they range in adult size from the mouse-size Microcebus (approximately 60 g) to the pony-size Gorilla (approximately 200 kg); some walk, trot, and gallop quadrupedally, others walk and run bipedally, some brachiate, some hop, some even use their tails during locomotion. Yet, taken as a whole, animals of all classes represent a much larger size range, and have the same and more specializations for locomotion. In this chapter I will review some aspects of the energetics and mechanics of terrestrial (and arboreal) locomotion, and then compare in more detail both the primates as a group and a few of the more specialized primate species. Then it will be possible to compare the many different sizes, shapes, and modes of locomotion of the primates to those of the terrestrial vertebrates in general.

The low risk of colon cancer among the Japanese suggests their high intake of dietary fibre. Composite diet mixtures for 1959, 1970, and 1979 were prepared utilising the food consumption data from the National Nutrition Survey in Japan and analysed for non-starch polysaccharides (NSP) at the Dunn Clinical Nutrition Centre in Cambridge. The results showed that average intake of NSP by a Japanese in the above years did not exceed 13 g per day, which is as low as the corresponding intake by the Scandinavians and the British whose risk of colon cancer is known to be high. Since all the materials were analysed by the same methods and at the same laboratory, the results are well comparable and indicate that the low risk of colon cancer among the Japanese cannot readily be explained by their intake of NSP alone.

To define the role of insulin in blood pressure regulation, the hormone's action on renal sodium handling, potassium balance, pressor reactivity, and the release of catecholamines and aldosterone are summarized. Insulin-stimulated renal sodium reabsorption induces expansion of the extracellular volume, increase in cardiac output, and ultimately, hypertension. On the other hand, the insulin-induced shift of potassium into the cell interior is transient and appears to be of little consequence for long-term blood pressure control. Although the release of norepinephrine is stimulated by insulin, a norepinephrine-mediated pressor effect is prevented in healthy men by a simultaneous norepinephrine-antagonistic action of insulin. The latter causes the fall in blood pressure seen after intravenous insulin in patients with autonomic dysfunction who lack the rise in norepinephrine release. Both in healthy and in diabetic men, exogenous insulin does not modify the pressor effect of angiotensin II, although it impairs the secretion of aldosterone during stimulation by supraphysiological doses of angiotensin II.

There has been a considerable upsurge of interest recently in the concept of interspecific allometry (Gould, 1966), which relates to the scaling of individual characteristics to match body size in different species. Two particularly important developments have been taking place in theoretical aspects of allometry (e.g., see other contributions to this volume) and in the extension of allometric analysis to new fields of enquiry. One example of the application of allometric principles to an entirely new area of research is provided by the work conducted by Chivers and Hladik (1980) on the morphology of the gastrointestinal tract in primates and other mammals. Further development of this particular approach forms the subject of this chapter.

Huxley (1932) consolidated the study of allometry by providing a theoretical formulation of allometric growth and by analyzing many examples of allometric relationships, including the static allometry of adults within a population and the evolutionary allometry between populations and species. Unaided by an explicit theory connecting the different levels of allometry, Huxley (1932, pp. 212–224), Gould (1975, pp. 277–280), and others have attempted to suggest possible relationships between levels of allometry, usually by a simple extrapolation from one level to another.

In an earlier study (Preuschoft and Denies, 1984), we investigated the biomechanical advantages of the considerable arm length in brachiators—a wellknown phenomenon. We showed that longer arms increase traveling velocity in arm-swinging locomotion. In addition, it provides a quicker start and reduces the muscle force necessary to lift the body, i.e., reduces the energetic cost of locomotion. This seems to provide a fine explanation for why gibbons have long arms. Here we ask why these animals are not larger, and why their arms are not even more elongated.

The relative scaling of body parts to body size is an important consideration in modern primatology. Allometric studies allow investigation of changes in shape that occur in conjunction with changes in body size separately from those independent of body size change, the latter often a result of significant new adaptations (Aiello, 1981; Gould, 1975).

The cranium of living primates fascinates scientists of many different persuasions. As an experimental system, it serves as test-bed for craniofacial medical procedures; as an evolutionary sketchbook, it aids in solving certain questions of comparative functional anatomy and posing others.

The ratio of actual cost to least-cost expenditure on nutrition is shown to increase with income.

The two great syntheses that established the study of allometry were D’Arcy Thompson’s (1917, 1942, 1961) On Growth and Form and Julian Huxley’s (1932) Problems of Relative Growth. The bulk of Thompson’s volume dealt with the mechanical and physical factors underlying shape transformation. In his chapter entitled “The rate of growth, ” however, Thompson (1942, p. 79) stressed that “the form of an organism is determined by its rate of growth in various directions; hence rate of growth deserves to be studied as a necessary preliminary to the theoretical study of form.” Huxley’s (1932) work built on Thompson’s foundation through extensive empirical and theoretical investigations of relative, or differential, growth in organisms. Huxley showed that a simple power function, Y = bX k , could often describe correlated changes between growing parts (X and Y) of the body. He also analyzed ontogenetic allometry (relative growth, or heterogony, as Huxley labeled it) in terms of growth gradients, taxonomy, genetics, and evolutionary transformations. Huxley’s approach to the study of size and shape, there fore, was explicitly rooted in the analysis of growing form; we often term this growth allometry, in order to distinguish it from size allometry, which focuses on allometric changes in static adult series (Simpson, et al., 1960).

The study of cranial variation has played an important role in primate systematics. Many different research strategies have been employed to investigate functional anatomy of the mammalian skull; but to fully understand the adaptive significance of cranial structure, it is necessary to consider cranial allometry, the relationship between the size and shape of the skull and body size. Over 20 years ago, le Gros Clark (1963, pp. 156–157) noted that It is of the utmost importance to understand the implications of allometry in evolutionary development as well as in the growth of the individual.. As the result of allometric growth, the general shape and proportions of the skull (and also of other parts of the skeleton) may be very different in two quite closely related types. Such differences clearly have no great taxonomic value, since they may be related only to one major factor, i.e. body size.

Analysis of organ weight allometry in primates has been largely confined to examination of brain weight scaling [see Gould (1975) and references therein]. This emphasis reflects our quite natural interest in the unique degree of cerebral development in primates in general and in our species in particular. The scaling of the other internal organs (e.g., heart, lungs, kidneys) has received far less attention, however. Only a handful of studies have addressed the question of primate soft tissue allometry. These include Stahl (1965) and Stahl and Gummerson (1967) on interspecific organ weight allometry; Gest and Siegel (1983) and Larson (1978) on intraspecific organ weight scaling among adult olive baboons and stumptail macaques, respectively; and Snow and Vice (1965) and Stahl et al. (1968) on ontogenetic organ weight allometry in olive baboons and howler monkeys, respectively. Though all represent valuable contributions, to answer general questions about organ weight allometry, such as whether all primate species share a common developmental pattern, or if some species possess unique specializations in terms of the size of certain organs, we require a broad, comparative data base in order to discern regular patterns and recognize special cases. The present study represents an effort to supply such a data base. It examines the ontogenetic scaling of nine internal organs in each of six primate species. The importance of studying ontogentic trends has been emphasized in several recent papers (e.g., Alberch et al., 1979; Jungers and Fleagle, 1980; Shea, 1981). These authors have shown that understanding the developmental patterns of related species can be an extremely useful aid in determining their phylogenetic relationships

Secondary sexual differentiation in sexually reproducing organisms leads to more or less pronounced sexual dimorphism in an array of interrelated morphological, physiological, and behavioral features. Among primates morphological sexual differences occur in a wide range of characteristics, including (1) size (body weight and linear body dimensions such as trunk, head, and tail length), (2) dentition (such as canine size), (3) cranial features (such as prognathism, or sagittal and nuchal cresting), (4) locomotor apparatus (dimensions of axial and appendicular skeleton, muscular development), (5) internal organs (such as brain and heart size), (6) external features (such as pelage color and markings, shoulder capes and manes, permanent skin ridges, and coloration, particularly on the face), and (7) maturational, seasonal, or periodic morphological changes associated with reproductive cycles (Leutenegger, 1982a).

Living primates vary in size from species averaging less than 100 g to some averaging well over 100 kg (Fig 1). The fossil record provides evidence of both much larger and much smaller species (e.g., Fleagle, 1978; Gingerich et al., 1982; Gunnell, 1983; Simons and Ettel, 1970). There is no doubt that much of the diversity that these species show in structure, physiology, behavior, and ecology is intimately related to differences in body size (e.g., Schmidt-Nielson, 1975; Clutton-Brock and Harvey, 1983). The details of this relationship are the domain of allometry. Thus, in its broadest sense, allometry is the study of the relationship between size and adaptation.

Among primates, the extent of sexual dimorphism in body size ranges from species where mature females are slightly larger than mature males, as in some of the marmosets and tamarins (Ralls, 1976), through species where males are slightly larger than females, like many of the diurnal lemurs and the arboreal colobines, to those where males are nearly twice as heavy as females, as in the larger cercopithecines, the gorilla and the orang (Clutton-Brock and Harvey, 1978). The tendency for polygynous mammals to show greater size dimorphism than monogamous ones was originally noticed by Darwin (1871), and quantitative studies have subsequently confirmed that in primates (Gautier-Hion, 1975; Clutton-Brock et al., 1977; Clutton-Brock and Harvey, 1978) (see Fig. 1), pinnipeds and ungulates (Alexander et al., 1979), as well as birds (Lack, 1968) and amphibians (Shine, 1979) monogamous species consistently show less dimorphism than polygynous ones.

Ramapithecus punjabicus, Sivapithecus indiens, and Gigantopithecus bilaspurensis are three mediumto large-sized apes from the middle Miocene (about 8–10 mya). In recent years, one or another of these species has been proposed to be the earliest known hominid (Simons, 1977; Kay, 1982), a common ancestor of all modern hominids and great apes (Greenfield, 1980), closely related to the ancestory of the orangutan (Andrews and Cronin, 1982; Landau et al., 1982), or perhaps a side branch with no modern descendants (Zihlman and Lowenstein, 1979). These species are best known from deposits in Pakistan and India, and almost exclusively as teeth and facial bones. Their interrelationships are controversial, recent workers suggesting that R. punjabicus and S. indicus are simply males and females of a single species (de Bonis and Melentis, 1980), separate species from one genus (Greenfield, 1979; Andrews

In his study of the Allied blockade of 1915-1919, Vincent examines the rationale and impact of this first large-scale use of food as a weapon in the twentieth century. Vincent demonstrates that the collapse of the German war effort was induced as much by prolonged hunger as by military reversal. Under blockade since 1915, the starving Germans were, by 1918, in a state of growing anarchy. Remarkably, however, the armistice ending hostilities specifically required the continuation of the blockade until such time as German signatures had been affixed to a peace treaty.

The intent of this chapter is to examine the question of whether and how tooth size scales to body size in a living human population, and to determine the relationship that such intrapopulational scaling might have to the explanation and general understanding of the tooth size—body size relationship. In the process of this examination, focus is brought to the concept of allometry, its basis in fact and theory, the question of whether it is a descriptive or an explanatory device, and its potential for modeling the tooth size—body size relationship.

Thirty-five patients who had suffered from bronchial asthma for an average of 12 yr, all receiving long-term medication, 20 including cortisone, were subject to therapy with vegan food for 1 yr. In almost all cases, medication was withdrawn or drastically reduced. There was a significant decrease in asthma symptoms. Twenty-four patients (69%) fulfilled the treatment. Of these, 71% reported improvement at 4 months and 92% at 1 yr. There was a significant improvement in a number of clinical variables; for example, vital capacity, forced expiratory volume at one sec and physical working capacity, as well as a significant change in various biochemical indices as haptoglobin, IgM, IgE, cholesterol, and triglycerides in blood. Selected patients, with a fear of side-effects of medication, who are interested in alternative health care, might get well and replace conventional medication with this regimen.

Prolonged exercise in the fasted state frequently results in a lowering of blood glucose concentration, and when the intensity is moderate (i.e. 60-80% of VO2 max), muscle often becomes depleted of glycogen. The extent to which carbohydrate feedings contribute to energy production, and their effectiveness for improving endurance during prolonged exercise, are reviewed in this article. Prolonged exercise (i.e. greater than 2 hours) results in a failure of hepatic glucose output to keep pace with muscle glucose uptake. As a result, blood glucose concentration frequently declines below 2.5 mmol/L. Despite this hypoglycaemia, fewer than 25% of subjects display symptoms suggestive of central nervous system dysfunction. Since fatigue rarely results from hypoglycaemia alone, the effectiveness of carbohydrate feeding should be judged by its potential for muscle glycogen sparing. Carbohydrate feeding during moderate intensity exercise postpones the development of fatigue by approximately 15 to 30 minutes, yet it does not prevent fatigue. This observation agrees with data suggesting that carbohydrate supplementation reduces muscle glycogen depletion. It is not certain whether carbohydrate feeding increases muscle glucose uptake throughout moderate exercise or if glucose uptake is higher only during the latter stages of exercise. In contrast to moderate intensity exercise, carbohydrate feeding during low intensity exercise (i.e. less than 45% of VO2 max) results in hyperinsulinaemia. Consequently, muscle glucose uptake and total carbohydrate oxidation are increased by approximately the same amount. The amount of ingested glucose which is oxidised is greater than the increase in total carbohydrate oxidation and therefore endogenous carbohydrate is spared. The majority of sparing appears to occur in the liver, which is reasonable since muscle glycogen is not utilised to a large extent during mild exercise. Although carbohydrate feedings prevent hypoglycaemia and are readily used for energy during mild exercise, there is little data indicating that feedings improve endurance during low intensity exercise. When the reliance on carbohydrate for fuel is greater, as during moderate intensity exercise, carbohydrate feedings delay fatigue by apparently slowing the depletion of muscle glycogen.

The concentration of high density lipoproteins (HDL) is related to the catabolism of triglyceride-rich lipoproteins. In order to elucidate the mechanisms by which alcohol increases plasma HDL levels we measured the turnover kinetics of very low density lipoprotein (VLDL) triglycerides in 10 alcoholic men without liver disease and in nonalcoholic control men matched for age, weight and plasma VLDL triglyceride level. The study was repeated in the alcoholics after a 2-week abstinence period. The alcoholic men had elevated HDL cholesterol but reduced low density lipoprotein (LDL) cholesterol as compared to the controls. The fractional catabolic rate and the total turnover (production) rate of VLDL triglycerides were both significantly increased (P less than 0.05) in the alcoholic men before abstinence. After withdrawal of alcohol both the synthetic rate and the catabolic rate of VLDL triglycerides returned to normal and the HDL (HDL2 and HDL3) cholesterol fell. The per cent decrease in HDL2 cholesterol during abstinence was positively correlated to the respective fall of VLDL triglyceride fractional catabolic rate (r = +0.51). The results suggest that the absence of hypertriglyceridemia and the elevated levels of HDL in regular alcohol users may be partly based on increased metabolic clearance of VLDL particles and on subsequent accelerated transfer of the VLDL surface components to HDL.

We examined the effects of high-carbohydrate and high-fat diets on the serum lipid levels of distance runners. For seven days before each study, subjects consumed a diet containing 15% protein, 32% fat, and 53% carbohydrate. During 14-day experimental periods, a control group (n = 10) continued the same diet while two other groups consumed 69% of their calories as either carbohydrate (n = 13) or fat (n = 14). High-density lipoprotein (HDL)-cholesterol decreased 9% during the high-carbohydrate diet because of a 26% fall in the HDL2 fraction (1.063 to 1.125 g/mL). These changes were not accompanied by changes in the levels of apolipoproteins (apo) A-I or A-II. Total and low-density lipoprotein (LDL)-cholesterol initially decreased but subsequently exceeded pre-diet values while triglyceride concentrations increased 30% to 50%. Postheparin lipoprotein lipase activity (LPLA) fell 20%. Despite these dietary effects, HDL and HDL2 cholesterol concentrations in the athletes remained above values typical of sedentary men. The high-fat diet produced different effects on the serum lipids and lipoprotein levels of the athletes. HDL levels changed little during the study although HDL-cholesterol and apo A-I on the last diet day were both slightly above initial values. The high-fat diet provided 111 g of saturated fat per day but had surprisingly little effect on total and LDL-cholesterol whereas serum triglycerides fell by 10% to 20%. Postheparin LPLA increased 30% with fat feeding and the changes in LPLA correlated with alterations in triglyceride levels (r = -0.53, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

The objective of the Rationale of the Diet-Heart Statement of the American Heart Association was to restate the diet-heart recommendations of the American Heart Association and to quote the original publications on which they are based. Examination of those publications reveals that for the most part, they are obsolete or misquoted. The last section of the Rationale concerns the role of genetics and very briefly reviews the epidemiological and dietary intervention trial evidence. The latter discussion may be summarized as meaning that risk levels are in the 90 percentile group of plasma cholesterol levels and that those levels are due to genetic factors which "dietary changes alone cannot normalize." It admits that "all" dietary intervention trials "were flawed in one or another aspect of experimental design." Hope is expressed that the Multiple Risk Factor Intervention Trial and the Lipid Research Clinics Primary Prevention Trial will support the diet-heart theory. The former did not and the latter was designed to test cholestyramine and not diet.

The objective of the Rationale of the Diet-Heart Statement of the American Heart Association was to restate the diet-heart recommendations of the American Heart Association and to quote the original publications on which they are based. Examination of those publications reveals that for the most part, they are obsolete or misquoted. The last section of the Rationale concerns the role of genetics and very briefly reviews the epidemiological and dietary intervention trial evidence. The latter discussion may be summarized as meaning that risk levels are in the 90 percentile group of plasma cholesterol levels and that those levels are due to genetic factors which "dietary changes alone cannot normalize." It admits that "all" dietary intervention trials "were flawed in one or another aspect of experimental design." Hope is expressed that the Multiple Risk Factor Intervention Trial and the Lipid Research Clinics Primary Prevention Trial will support the diet-heart theory. The former did not and the latter was designed to test cholestyramine and not diet.

The effect of intervention with a lacto-ovo vegetarian diet on serum concentrations of cholesterol, triglyceride, total high-density lipoprotein cholesterol (HDL-C), HDL2-C, HDL3-C, low-density lipoprotein cholesterol, apoprotein-B, apoprotein-HDL, and Lp(a) was studied in 19 men and 17 women. Most weekday meals were obtained from a single source and dietary records were completed to assess the changes in nutrient intakes. Blood was collected in the 6th wk of each dietary period. Because of strong correlations between many of the changes in nutrient intakes, principal component (factor) analysis was used followed by stepwise multiple regression analysis to identify associations between changes in diet and changes in lipid, lipoprotein or apoprotein levels. Three principal components accounted for 92.0% of the variation in lipid levels: factor 1 represented an increase in saturated fat, total fat, monounsaturated fat, cholesterol, and energy intake: factor 2 represented an increase in fiber and polyunsaturated fat, and decrease in protein intake; factor 3 an increase in total carbohydrate, complex carbohydrate, and energy intake. Where a change in a variable was significantly associated with change in diet, one factor appeared primarily responsible for the change; total cholesterol (factor 2, p = 0.034); triglyceride (factor 3, p = 0.005); apo-HDL (factor 1, p = 0.014); HDL2-C (factor 2, p = 0.023), HDL3-C (factor 3, p = 0.015). A borderline significant association was seen for total HDL-C (factor 2, p = 0.055).

Hypertensive patients had higher levels of linoleic acid (LA) in serum lipids than normal controls. Administration of large doses of LA failed to raise the percentage of its metabolite arachidonic acid (AA) in serum lipids. Similarly, intake of large amounts of alpha-linolenic acid (alpha-LNA) failed to increase the amount of eicosapentaenoic acid (EPA). The percentage of EPA in serum lipids could readily be increased by direct administration of comparably low doses in a mackerel diet. Hypertensive subjects seem to desaturate and elongate LA and alpha-LNA only very slowly.

This paper reviews the association between a vegetarian diet and a number of risk factors for cardiovascular disease investigated in a series of epidemiological and experimental studies. Ninety-eight Seventh-day Adventist "vegetarians" were similar to 113 Mormon omnivores for strength of religious affiliation, consumption of alcohol, tea and coffee and use of tobacco, but were significantly less obese and had significantly lower blood pressures adjusted for age, height and weight. A random sample of forty-seven Adventist vegetarians had significantly lower home blood pressures, serum cholesterol levels and blood pressure responses to a cold-pressor test than Mormon omnivores carefully matched for age, sex and Quetelet's index. In a controlled dietary intervention study mean systolic and diastolic blood pressures and serum cholesterol fell significantly during feeding with a vegetarian diet--an effect unrelated to changes in other lifestyle factors. Dietary analysis indicated that a vegetarian diet provided more polyunsaturated fat, fibre, vitamin C, vitamin E, magnesium, calcium and potassium and significantly less total fat, saturated fat and cholesterol than an omnivore diet. There was no evidence for a difference between vegetarians and omnivores in levels of catecholamines, plasma renin activity, angiotensin II, cortisol or serum and urinary prostanoids.

Twenty-nine patients who had suffered from essential hypertension for an average of 8 years, all receiving long-term medication for hypertension, were subject to therapy with vegan food for 1 year. In almost all cases medication was withdrawn or drastically reduced. There was a significant decrease in systolic and diastolic blood pressure. A number of reported symptoms disappeared. There was a significant improvement in a number of clinical variables as well as a significant change in various biochemical indices such as urea, haptoglobin, cholesterol and triglyceride concentrations in blood. Subjectively all patients reported improvement. Selected patients, with a fear of side-effects of medication, who are interested in alternative health care might replace conventional medication with this dietary regimen.

The effect of ketone bodies on glucose production (Ra) and utilization (Rd) was investigated in the 24-h starved, conscious unrestrained miniature pig. Infusing Na-DL-beta-OH-butyrate (Na-DL-beta-OHB) and thus shifting the blood pH from 7.40 to 7.56 resulted in a decrease of Ra by 52% and of Rd by 45%, as determined by the isotope dilution technique. Simultaneously, the concentrations of arterial insulin and glucagon were slightly enhanced, whereas the plasma levels of glucose, lactate, pyruvate, alanine, alpha-amino-N, and free fatty acids (FFA) were all reduced. Infusion of Na-bicarbonate, which yielded a similar shift in blood pH, did not mimick these effects. Infusion of equimolar amounts of the ketoacid, yielding a blood pH of 7.35, induced similar metabolic alterations with respect to plasma glucose, Ra, Rd, and insulin; however, plasma alanine and alpha-amino-N increased. Infusing different amounts of Na-DL-beta-OHB resulting in plasma steady state levels of ketones from 0.25 to 1.5 mM had similar effects on arterial insulin and glucose kinetics. No dose dependency was observed. Prevention of the Na-DL-beta-OHB-induced hypoalaninemia by simultaneous infusion of alanine (1 mumol/kg X min) did not prevent hypoglycemia. Infusion of Na-DL-beta-OHB plus insulin (0.4 mU/kg X min) showed no additive effect on the inhibition of Ra. Ketones did not inhibit the insulin-stimulated metabolic clearance rate (MCR) for glucose. Infusion of somatostatin (0.2 micrograms/kg X min) initially decreased plasma glucose, Ra, and Rd, which was followed by an increase in plasma glucose and Ra; however, on infusion of somatostatin plus Na-DL-beta-OHB, hypoglycemia and the reduced Ra were maintained. In the anaesthetized 24-h starved miniature pig, Na-DL-beta-OHB infusion decreased the hepatic exchange for glucose, lactate, and FFA, whereas the exchange for glycerol, alanine, and alpha-amino-N as well as liver perfusion rate were unaffected. Simultaneously, portal glucagon and insulin as well as hepatic insulin extraction rate were elevated. Leg exchange for glucose, lactate, glycerol, alanine, alpha-amino-N, and FFA were decreased, while ketone body utilization increased. Repeated infusion of Na-DL-beta-OHB at the fourth, fifth, and sixth day of starvation in the conscious, unrestrained mini-pig resulted in a significant drop in urinary nitrogen (N)-excretion. However, this effect was mimicked by infusing equimolar amounts of Na-bicarbonate. In contrast, when only the ketoacid was given, urinary N-excretion accelerated. To summarize: (a) Ketone bodies decrease endogenous glucose production via an insulin-dependent mechanism; in addition, ketones probably exert a direct inhibitory action on gluconeogenesis. The ketone body-induced hypoalaninemia does not contribute to this effect. (b) The counterregulatory response to hypoglycemia is reduced by ketones. (c) As a consequence of the decrease in R(a), glucose utilization declines during ketone infusion. (d)The insulin-stimulated MCR for glucose is not affected by ketones. (e) Ketones in their physiological moiety do not show a protein-sparing effect.

Of 299 obese children who visited our obesity clinics, 36 were found to have elevated levels of serum transaminases by routine laboratory examination. Liver biopsy was carried out in 11 children. Based on the criteria of Adler and Schaffner (1979), the biopsy specimens were studied histologically. As a result, fatty liver (Group I) was observed in three patients, fatty hepatitis (Group II) in two, fatty fibrosis (Group III) in five, and fatty cirrhosis (Group IV) in one. The duration of obesity, but not its degree, was considered to be related to the extent of fibrosis. Accordingly, we concluded that the fatty liver of simple obesity in children may progress to liver cirrhosis and that childhood obesity should be treated as early as possible.

When exposed to hypoxia, intact mice, with elevated blood ketones, live longer than mice with normal blood ketones. To evaluate a possible mechanism responsible for this phenomenon a rat brain slice preparation was used to determine if brain tissue would utilize glucose or ketones preferentially during exposure to reduced oxygen. Reducing available oxygen in the incubation medium from 95%, in steps, to 5% produced the expected gradual reduction in the carbon dioxide formation from glucose. In contrast, reducing the oxygen level to 40 and 20% resulted in a statistically significant stimulation of the production of carbon dioxide from the ketone beta-hydroxybutyrate. At very low oxygen levels carbon dioxide production from either substrate was reduced. These results are consistent with the hypothesis that ketones can be used in addition to glucose as a substrate for brain energy production even during reduced oxygen availability. If the increase in carbon dioxide production from ketones can be equated with an increase in energy production from this supplemental substrate then ketones may be therapeutically useful in avoiding the collapse of brain function during moderate hypoxia.

A 12-year old boy suffered episodes of vomiting, lethargy, and hypoglycaemia from the age of 1 year. Adhering to a vegetarian diet caused an increase in frequency and severity of the attacks. It was found that he was suffering from systemic carnitine deficiency that responded promptly to treatment with L-carnitine.

A 12-year old boy suffered episodes of vomiting, lethargy, and hypoglycaemia from the age of 1 year. Adhering to a vegetarian diet caused an increase in frequency and severity of the attacks. It was found that he was suffering from systemic carnitine deficiency that responded promptly to treatment with L-carnitine.

The influence of soy protein isolate (SPI) in the diet on whole-body retention of extrinsically radiolabeled iron from test meals containing or not containing SPI was evaluated in marginally iron-deficient weanling rats. In experiment 1 SPI was compared with casein in a 2 X 2 factorial design: diets and test meals were either SPI-based or casein-based. Diets were fed for 13 days prior to the test meal and for 7 days subsequent to the test meal. Rats fed the SPI-based diet retained less iron from test meals than did rats fed the casein-based diet (66.1 vs. 74.8%, P less than 0.01). Experiment 2 showed that an SPI-based diet fed during the final 4 days of a 14-day pre-test meal period and subsequent to the test meal led to less iron retention compared to a casein-based diet. In addition to the observed diet effect, experiment 1 showed that iron retention was less from an SPI-based test meal than from a casein-based test meal, confirming previous reports of adverse effects of SPI on iron retention. The present experiments show that SPI can adversely affect from retention in two ways: by its presence in the diet before and after a test meal, and by its presence in a test meal.

Eighty-seven male Sprague-Dawley rats (245-300 g) were randomly assigned to one of two experimental groups. The first group consumed a diet high in fat and low in carbohydrate (LCD), whereas the second group ate a normal diet (ND). After either 1 or 5 wk on the diets, rats from each group were killed either before or after an exhausting run on a rodent treadmill (35 m X min-1, 0% grade). The LCD animals ran significantly longer before exhaustion at both week 1 (44.9 +/- 5.1 vs. 41.6 +/- 4.2 min) and week 5 (47.1 +/- 3.6 vs. 35.5 +/- 3.1 min) (P less than 0.05). Adaptations to the LCD included lower muscle and liver glycogen content, decreased rate of glycogen breakdown during exercise, decreased lactate production, and elevated blood ketone levels. In addition to these substrate changes, the LCD caused increased enzyme activities of muscular 3-hydroxyacyl-CoA dehydrogenase (35-110%) and citrate synthase (15-20%). These data indicate that rats exposed to a high-fat diet are capable of prolonged intense exercise in spite of limited glycogen stores. This improved capacity for exercise appears to be partially the result of muscular adaptations to the diet, which apparently increase the ability to oxidize fat and concomitantly spare glycogen.

Persons who use tables of food composition have often found that foods that vegetarians commonly eat are not included. To help remedy this situation, a table is presented which includes the 49 foods on the vegetarian Exchange Lists and 18 additional nonmeat foods. Nutrient contents of household measures of these foods are given for water, protein, fat, carbohydrate, calcium, phosphorus, iron, potassium, zinc, vitamin A, thiamin, riboflavin, niacin, vitamin C, and folacin. Nutrient amounts were derived from USDA sources and from other published research when available. Nutrient amounts from foods assumed to be identical to those in the table were placed in parentheses. When nutrient amounts were not available, they were estimated from similar foods and placed in brackets. When values found for a single nutrient in a food varied by 20% or more, the total range was shown. When a dash was found in a literature reference and the amount of the nutrient was known to be insignificant, a zero was presented in the table. Thus, there are no gaps in the table. Until accurate laboratory-derived data are available for the nutrients in vegetarian foods, this table, used with appropriate judgment, should be useful for estimating the nutrient intakes of persons who eat vegetarian foods.