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PubMed1988

Dehydroepiandrosterone therapeutics: acetylation of DHA in mouse liver.

This investigation was designed to evaluate the possibility that the therapeutic benefits of dehydroepiandrosterone (DHA)-feeding in mice is mediated by (1) a metabolite of DHA formed in liver or (2) by way of the obligatory hepatic metabolism of DHA fed in large amounts. We found that the pattern of metabolism of DHA is strikingly different when DHA in low (tracer) quantities is incubated with mouse liver compared with that found when DHA in high concentrations is incubated with this tissue. In the former case, the principal metabolites are sulfoconjugates and other polar compounds, e.g. hydroxylated products. In the case of DHA metabolism when the substrate is present in high concentrations (1-100 microM), the principal metabolite formed is delta 5-androstenediol. And in this case, there is the formation of very nonpolar metabolites, which we have identified as the acetates of DHA and delta 5-androstenediol. We find further that the acetates are formed by a transacetylation mechanism in which performed acetylated compounds, e.g. pregnenolone acetate and ethyl acetate, can serve directly as co-substrates; but (at least in short-term incubations), Na+-acetate and acetyl CoA do not serve as co-substrates. We suggest that the therapeutic benefits of DHA-feeding in mice may be, in part, the result of alterations in hepatic intermediary metabolism that is obliged by the metabolism of DHA when this otherwise inert agent is fed in large amounts. Thus, DHA-feeding may serve to cause changes similar to those that are beneficial or therapeutic with dietary manipulations including caloric restriction.

Acetylation↗

PubMed1978

Serum thyroid hormone concentrations during prolonged reduction of dietary intake.

In nine obese but otherwise healthy subjects the effect of caloric restriction on the serum concentrations of thyroxine (T4), 3,3',5-triiodothyronine (T3), 3,3',5'-triiodothyronine (rT3), urea, uric acid, creatinine, and bilirubin was studied. Blood was obtained before and 2, 4, and 6 wk after the subjects had changed to a chemically defined diet (31 g amino acids, 44 g carbohydrate, and 1.5 g fat; 300 kcal/day). A decline of body weight to 88% and of serum T3 to 70% of the pretreatment values was observed. Creatinine and bilirubin increased to 115% and 163%, respectively. Uric acid and rT3 showed a transient rise to 148% and 180%, respectively. Serum urea was lowest (72%) from the second until the fourth week. There was a highly significant correlation between serum rT3 and uric acid (r = 0.77, p less than 0.001). The time course of the changes seems to indicate that conversion of T4 into T3 and rT3 is mediated by separate processes.

Adult↗

PubMed1983

Hypothermia in a patient with anorexia nervosa.

A young woman with anorexia nervosa had severe recurrent hypothermia. Initial evaluation revealed a thiamine deficiency. Administration of pharmacologic doses of thiamine improved voluntary food intake, and her temperature normalized. Following the restoration of body weight, withdrawal of supplemental thiamine produced a clinical relapse. After reinstitution of supplemental thiamine, the patient again became asymptomatic until she chose to consume a calorically-restricted diet. With progressive weight loss, hypothermia recurred and was unresponsive to thiamine therapy. Fortuitously, the patient's intake of sucrose was abruptly increased, and her body temperature normalized within seven days. The potential roles of thiamine and carbohydrate in thermoregulation are discussed.

Adult↗

PubMed1992

Potentiation of the thermogenic antiobesity effects of ephedrine by dietary methylxanthines: adenosine antagonism or phosphodiesterase inhibition?

Current concepts about the mechanisms underlying the therapeutic effects of dietary methylxanthines (caffeine, theophylline, and theobromine) favor their actions as antagonists of adenosine receptors, and attribute their other possible modes of action, namely those associated with translocation of intracellular calcium, inhibition of phosphodiesterase enzyme (PDE) activity, or the release of catecholamines, to high (near-toxic) doses. From studies measuring the respiration rate of brown adipose tissue (BAT), evidence is provided here that at concentrations compatible with therapeutic doses, the ability of methylxanthines (25 to 50 mumol/L) to potentiate the thermogenic effect of the sympathomimetic drug, ephedrine (0.25 mumol/L), particularly under conditions of caloric restriction, involves a minor contribution of adenosine antagonism, but could mainly be explained by the inhibition of PDE activity. In view of current interest in the pharmacological stimulation of metabolic rate to assist the management of obesity with low-calorie regimens, the targeting of PDE activity is therefore a rational approach in the search for drugs that could potentiate sympathomimetic stimulation of metabolic rate.

Adenosine↗

PubMed1994

The effects of weight loss by exercise or by dieting on plasma high-density lipoprotein (HDL) levels in men with low, intermediate, and normal-to-high HDL at baseline.

To assess whether baseline plasma high-density lipoprotein (HDL) cholesterol levels affected the HDL response to weight loss, we examined lipoprotein changes in overweight men aged 30 to 59 years who were randomized to lose weight by exercise training (primarily running, n = 46) or by caloric restriction (ie, dieting, n = 42) or to remain sedentary, nondieting controls (n = 42) in a 1-year study. In exercisers, absolute increases in HDL (mg/dL) were greatest in men with normal-to-high baseline HDL and least in men with low baseline HDL. Specifically, when divided into groups of low (< or = 37 mg/dL), intermediate (38 to 47 mg/dL), and normal-to-high HDL cholesterol (> or = 48 mg/dL) at baseline, the exercisers increased HDL cholesterol by 2.3 +/- 1.9, 4.9 +/- 1.1, and 7.0 +/- 1.3 mg/dL, respectively; HDL2 cholesterol by 0.8 +/- 1.6, 2.3 +/- 1.2, and 5.1 +/- 1.3 mg/dL; and HDL2 mass by 2.8 +/- 5.1, 9.5 +/- 8.9, and 31.7 +/- 11.0 mg/dL. Relative increases in HDL cholesterol were more similar in the low (7.1% +/- 6.1%), intermediate (12.4% +/- 3.9%), and normal-to-high men (13.2% +/- 4.0%). Regression analyses were performed to assess whether baseline HDL cholesterol was related to the amount of absolute HDL change per unit of weight loss. In exercisers, the increase in HDL3 cholesterol concentrations was significantly greater in men with low HDL than in those with normal-to-high HDL at entry (2.0 +/- 0.8 v 0.2 +/- 0.8 mg/dL per kg/m2 lost).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1995

Effects of weight loss on norepinephrine and insulin levels in obese older men.

Older individuals have higher plasma insulin and norepinephrine (NE) levels than the young. This may be due to biological aging; however, these changes also may be due in part to the increase in abdominal obesity that often accompanies aging. The latter possibility was tested by examining the effects of weight loss on plasma insulin and NE levels in 11 healthy men aged 52 to 72 years who had mild to moderate obesity (body mass index [BMI], 27 to 36 kg/m2). Plasma insulin levels were measured during an oral glucose tolerance test, and on a second day NE levels were measured during supine rest and upright posture. Subjects lost 10 +/- 5 kg (mean +/- SD) and decreased their waist to hip ratio ([WHR] an index of the pattern of regional fat distribution) 2.8% (P < .01) over 9 +/- 3 months through mild caloric restriction. This resulted in a 23% decrease (P < .05) in fasting insulin levels and a 48% decrease (P < .01) in 2-hour insulin levels. Weight loss also resulted in a 31% decrease (P < .001) in supine plasma NE levels and an 8% decrease (P < .05) in supine diastolic blood pressure (BP). Decreases in supine plasma NE levels correlated with changes in WHR (r = .61, P < .05), but did not correlate with changes in other measures of body composition or with changes in glucose and insulin levels. These results suggest that higher plasma NE levels are related to the distribution of body fat to upper-body or abdominal sites in obese older men.

Aged↗

PubMedDate not supplied

Dietary modulation of DNA damage in human.

Manipulation of human diet can modulate urinary biomarkers of oxidative DNA base damage (UBODBD), reflecting changes in levels of DNA damage. When dietary composition is maintained but caloric intake is decreased (caloric restriction), UBODBD excretion is suppressed. At isocaloric dietary intake the level of damage depends on diet composition. For diets consisting of foods containing carbohydrates, proteins, and fats but lacking fruits and vegetables, the level of damage is higher than for diets including fruits and vegetables, which are rich in natural antioxidants. Assay of urinary biomarkers is suggested as a potential test for quantitative assessment of the carcinogenic or anticarcinogenic properties of foods, food components, and diets and for individual responses to nutritional regimens.

Biomarkers↗

PubMed1986

The effects of repeated cycles of weight loss and regain in rats.

This study examined the metabolic effects of weight cycling, i.e., repeated periods of weight loss followed by regain. There were three groups of adult, male Sprague-Dawley rats: (1) Chow Controls (a normal weight control group fed chow throughout); (2) Obese Controls (animals fed a high-fat diet throughout); and (3) Obese Cycling (obese animals cycled through two bouts of caloric restriction and refeeding). The cycled animals showed significant increases in food efficiency (weight gain/kcal food intake) in the second restriction and refeeding periods compared to the first, i.e., weight loss occurred at half the rate and regain at three times the rate in the second cycle. Several physiological changes were associated with this cycling effect. At the end of the experiment, cycled animals had a four-fold increase in food efficiency compared to obese animals of the same weight who had not cycled. These data suggest that frequent dieting may make subsequent weight loss more difficult. The possible metabolic and health consequences of "yo-yo" dieting are discussed.

Adipose Tissue↗

PubMed1988

Behavioral and physiologic effects of early nutrition and social factors in the rat.

Two experimental methods to provoke caloric restriction during suckling were used. Each of the methods utilized two different rat groups: Low Growth (LG) and High Growth (HG). In one method, the groups also differed in a social factor, litter size: crowded (Cr) and control (Co). Growth differences and high levels of social competition were found among pups of the crowded group with Low Growth (CrLG) compared to the group with High Growth and small litters (CoHG). Both methods resulted in growth differences between respective groups from the first week of suckling. Differences in animal groups persisted forty days after weaning. LG animals had higher defecation scores with lower activity in the open-field test, higher susceptibility to restraint ulcers and adrenal hypertrophy than HG rats, in litters of equal size. However, early stimulation from social competition among pups in larger different litters in CrLG group counteracted nutritional factor effects. Elevated open-field defecation and ulceration scores with adrenal hypertrophy were found in CoHG rats.

Adrenal Glands↗

PubMed1991

Meal patterns of normal, untreated bulimia nervosa and recovered bulimic women.

In order to examine the meal pattern characteristics associated with bulimia nervosa the meal patterns of 19 untreated bulimia nervosa, 12 recovered bulimics, and 21 normal controls spontaneously eating in their natural environments were compared. Subjects reported in a diary everything they either ate or drank for seven consecutive days. Meal pattern correlations included comparisons of the groups in regard to meal size (and binge size), meal frequency, premeal and postmeal intervals, deprivation ratios, satiety ratios, stomach contents, and composition of meals and binges. Results indicated that, although total reported intake was normal, only 33% of the total calories consumed by the untreated bulimia nervosa subjects were not followed immediately by purging. Both purged and unpurged binges were twice as large as their meal sizes which did not differ from normal. It is hypothesized that the caloric restriction of the untreated bulimics is binge/purge specific, and is used by them as a form of weight control. The recovered group showed a lack of responsivity to the signals that influence meal size and intermeal intervals in normals including impaired social facilitation of eating. They also had larger meal sizes, and greater frequency of meals. It is theorized that recovered bulimics employ other, as yet unspecified, means of food intake restriction resulting in an abnormal feeding pattern.

Adolescent↗

PubMed1992

Obesity is the major cause of alterations in insulin secretion and calcium fluxes by isolated islets from aged rats.

To investigate the alterations in insulin secretion induced by aging, 2-month-old, 12-month-old, and 12-month old lean rats (submitted to a caloric restriction during the last month that causes a weight loss of approximately 20%) were studied. As expected, glucose intolerance and increased insulin response were observed during IV-GTT in 12-month-old rats. These effects were, however, reversed by weight loss. Insulin secretion was investigated in isolated islets both during static incubation and perifusion. In 12-month-old rats insulin secretion and 45Ca2+ efflux were lower only in the second phase of the hormonal secretion, suggesting an involvement of voltage-sensitive calcium channels in these phenomena. Considering that in vivo and in vitro alterations were reversed after weight loss, it is possible to conclude that obesity is probably a major cause of impaired insulin secretion in 12-month-old albino rats. Since 14C-glucose metabolism was not changed in islets from aged rats, the effect of obesity on insulin secretion is not due to altered glucose metabolism in pancreatic B-cells.

Aging↗

PubMed1984

Arresting development arrests aging in the nematode Caenorhabditis elegans.

Larval development of the nematode, Caenorhabditis elegans, can be arrested by either of two different treatment: (1) complete starvation, or (2) growth in a partially defined culture medium (axenic medium) of strains adapted to bacterial growth. The developmental arrest is complete under total starvation and the starved populations live about 10 days. The developmental block is incomplete in axenic medium; most animals mature but maturation takes 10 times longer than normal. If developmentally arrested cultures are returned to growth on E. coli, both the completely starved and the axenically arrested cultures mature at normal rates. Life-span is prolonged by 1 day for each day of complete starvation; life-span is prolonged by 0.7 days for each day of axenic arrest. These results suggest that aging and development are closely coupled in this system. The results are discussed in terms of previous observations on nutritional deprivation in other invertebrates and caloric restriction in mammals and are interpreted in light of theoretical models of senescence.

Aging↗

PubMed1990

Rats exposed prenatally to alcohol exhibit impairment in spatial navigation test.

Prenatal exposure to ethanol causes learning disabilities and low I.Q. scores. The objective of the present studies was to investigate whether exposure of rats to ethanol in utero, would induce a deficit in spatial memory in adult life. Pregnant rats were fed with an ethanol diet from day 1 of pregnancy till parturition. Control rats were either pair-fed with an isocaloric sucrose diet or were fed with lab-chow ad libitum. On the first day of birth, offspring exposed to ethanol in utero were placed with a control mother fed with lab-chow, while offspring of the lab-chow fed dams were placed with ethanol-treated dams. At 40, 60 and 90 days postnatally, behavioral testing was performed using the Morris swim maze, a test of spatial memory. Results indicated that the offspring exposed to ethanol in utero presented deficits in spatial memory processes. Ethanol did not completely block the learning of the swim maze task but the alcohol-exposed offspring exhibited longer latencies to perform the task, swam longer distances prior to locating and climbing onto the platform, and when the platform was removed, searched for it in all 4 quadrants of the pool. Restricted caloric intake during gestation and maternal behavior in early postnatal life also induced deficits in the performance on the swim maze task. However, these deficits were mild and short-lasting being absent at 60 and 90 days of age. In contrast, the deficits induced by ethanol were more severe and longer-lasting, being present in adult life.

Animals↗

PubMedDate not supplied

Gompertz mortality analysis: aging, longevity hormesis and toxicity.

The hazard function, denoted h(x), is the probability of death during an interval of time [Formula: see text], assuming survival to the beginning of the interval. Brues and Sacher provided both theoretical and experimental support for the assumption that h(x) is an exponential function of the mean intensity of physiologic injury for a homogeneous mammalian population provided an adequate diet, kept free of preventable disease and maintained under favorable, uniform conditions. Consequently, the Napierian logarithm of the hazard function, the 'Gompertzian', is proportional to the mean intensity of physiologic injury under the aforementioned conditions. Investigation of Gompertzian values therefore affords a simple and convenient measure of the mean population time course of aging, toxicity and beneficial life-enhancing effects (e.g., longevity hormesis and slowing of the aging process). (The word 'hormesis' has been applied to various forms of 'stimulation' elicited by low doses of otherwise toxic agents.) Using this method of analysis, reversible toxicity, reversible reduction in physiologic injury (longevity 'hormesis'), irreversible toxicity and irreversible reduction in aging (via caloric restriction) are all reviewed. It is demonstrated that these effects may superimpose upon one another, the most common combination following administration of mild to moderate doses of a toxic agent being irreversible toxicity combining with longevity hormesis.

Journal Article↗

PubMedDate not supplied

Processing of TRH precursor peptides in rat brain and pituitary is zinc dependent.

The enzymes responsible for the posttranslational processing of precursor proteins to form alpha-amidated peptide hormones require the availability of several cofactors, including zinc, copper and ascorbate ions. Major changes in the availability of these cofactors, as well as the rate of hormone precursor conversion to active hormone, occur during neonatal development, aging and caloric restriction. The effects of 6 weeks of a zinc-deficient (ZD1) diet, pair feeding (PF) and partial zinc deficiency (ZD6) compared to a control diet on the enzymatic cleavage and processing of prepro-TRH to form TRH have been studied in the hypothalamus, brain, and pituitary of young adult male Sprague-Dawley rats. Reverse phase high pressure liquid chromatography (HPLC) revealed that TRH was the major TRH-IR component of the hypothalamus, brain and pituitary. The effect of zinc deficiency on the TRH-Gly-IR HPLC profile of rat brain was to reduce selectively the are of the peaks for TRH-Gly and other low molecular weight pro-TRH peptide fragments with a C-terminal Gly compared to the corresponding TRH-Gly-IR peaks of the control group. We conclude that the processing of prepro-TRH to form TRH is zinc dependent via posttranslational processing enzymes such as carboxypeptidase H.

Amino Acid Sequence↗

PubMed1993

The Oslo Diet and Exercise Study (ODES): design and objectives.

The Oslo Diet and Exercise Study (ODES) is an unmasked randomized 2 x 2 factorial trial of 1-year duration for each participant. During 1990-1991 219 participants (198 males and 21 females) aged 41-50 were randomized into one of four treatment groups; no treatment (control), dietary changes alone, exercise alone, or a combination of the two treatments. At inclusion, the participants had no overt heart disease, but they had increased body weight; slightly increased blood pressure, serum triglycerides, and total cholesterol, and they had decreased HDL cholesterol. Further, they were all inactive at leisure time. The primary aim of the trial is to compare the isolated and combined effects of the four treatments on the variables fibrinogen, fibrinolytic capacity, coagulation factor VII, and platelet volume. A series of secondary hypotheses will also be tested, such as the effects on other coagulation and fibrinolytic components and activities; lipids and lipoproteins; fatty acids; glucose and insulin response to a glucose load; clinical, physiological, and anthropometric variables; and quality of life. The dietary treatments are adapted according to each participant's risk profile (level of total cholesterol, HDL cholesterol, triglycerides, blood pressure, and body weight). Fish and fish products are recommended. Special emphasis is put on caloric restriction in those who are overweight and those with elevated blood pressure. Exercise sessions take place three times a week under the guidance of highly qualified instructors. The aim is to increase peak oxygen uptake through aerobic endurance training. Adherence to the exercise program is monitored closely.

Adult↗

PubMed1994

Dietary regulation of mammary tumorigenesis in RIII/Sa mice: investigation of a possible mechanism.

The effects of caloric restriction on the incidence of mammary tumor development, the levels of the expression of mouse mammary tumor virus (MMTV)- and prolactin-RNA, as well as the levels of serum prolactin, were investigated in virgin RIII/Sa mice, a strain known to display a high incidence of spontaneous mammary tumor development. Of the 54 mice fed a low-calorie (LC; 10 kcal/day) diet containing low fat (LF; 5% corn oil) for a period of 72 weeks, only seven mice were found to develop mammary tumors, an incidence of 13%. By contrast, the cumulative tumor incidence in a similar sized group of mice, fed a high-calorie (HC; 16 kcal/day) low fat-containing diet was 73%. Estimation of the relative levels of MMTV-RNA, as determined by Northern and slot blot hybridizations, in the mammary glands of mice fed LCLF and HCLF diets for 8, 10, 16, 28, and 36 weeks revealed that the LCLF diet-fed mice expressed 4-15-fold less RNA than the HCLF diet-fed mice. Interestingly, however, the LCLF diet did not appear to exert any effect on the expression of prolactin RNA even though it reduced the levels of serum prolactin. We suggest that in RII/Sa mice the modulation of MMTV-induced mammary tumors by dietary calorie is linked to the secretion of serum prolactin which, in turn, affects the replication of MMTV required for mammary cell transformation.

Animals↗

PubMed1993

Homologous physiological effects of phenformin and chromium picolinate.

The insulin-sensitizing drug phenformin, in addition to its clinical utility in type II diabetes, has been reported to lower blood lipids, reduce body fat, enhance cellular immunity, and--in rodents--to increase mean lifespan and retard the development of growth of cancer. Initial studies with the insulin-sensitizing nutrient chromium picolinate indicate that it aids glucose tolerance in type II diabetes, lowers elevated LDL cholesterol, reduces body fat while increasing lean mass, and--in rats--increases median lifespan. These effects are thus analogous to those reported for phenformin; chromium picolinate should be tested to determine whether it likewise has a favorable impact on cellular immunity and cancer risk. The ability of both phenformin and chromium picolinate to increase lifespan suggests that age-related insulin resistance may play a profound role in the aging process. It may not be coincidental that caloric restriction--the best documented technique for increasing lifespan--markedly increases insulin sensitivity. Safe, appropriate measures for promoting lifelong insulin sensitivity include a low-fat diet, exercise training, and supplemental chromium picolinate.

Adipose Tissue↗