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Biomedical subjects

G N Wade

Publications and source records attributed to G N Wade.

At least 91 records · Page 5Linked to original sources
PubMed1983

Dietary obesity in golden hamsters: reversibility and effects of sex and photoperiod.

Golden hamsters fed a high-fat diet do not overeat, but they become obese because of decreases in energy expenditure. This decrease in actual energy expenditure is accompanied by increases in thermogenic capacity and brown adipose tissue mass, protein content, and DNA content. Three experiments examined this phenomenon in more detail. Experiment 1 demonstrated that this form of dietary obesity is largely reversible simply by returning the animals to a high-carbohydrate chow diet. However, the obesity which develops solely because of decreased energy expenditure is reversed primarily by decreased energy intake. In this respect fat-fed hamsters resemble tube-fed rats. Experiment 2 revealed that the effects of high-fat diet are at least as robust in female hamsters as in males. Experiment 3 examined the interactions between diet and photoperiod. Short days (10 hr light per 24 hr) had almost no effect on male hamsters fed Purina chow. However, nearly all of the effects of the high-fat diet (i.e., increases in body weight gain, feed efficiency, carcass energy content, percent ingested energy stored in the carcass, carcass lipid content, brown adipose tissue protein, and brown adipose tissue DNA) were exaggerated in hamsters housed in short days. High-fat-diet-induced increases in metabolic efficiency and thermogenic capacity may be of value in readying hamsters for winter. Furthermore, as winter approaches, decreasing day length might synergize with changes in diet quality to promote these beneficial changes in energy metabolism. Finally, fat-fed hamsters could be a useful animal model of some kinds of human obesity.

Adipose Tissue, Brown↗
PubMed1983

Copulatory behavior and hypothalamic estrogen and progestin receptors in chronically insulin-deficient female rats.

The effects of relatively short- or long-term diabetes on sexual receptivity and and proceptivity and on hypothalamic estrogen and progestin receptors were examined in rats fed regular chow or high fat diet. Ovariectomized, streptozotocin-induced chronically insulin deficient and normal rats received sequential treatments with 2 micrograms estradiol benzoate (EB) and 1 mg progesterone (P) 10 days following the induction of diabetes and were tested for lordosis and soliciting behaviors. Nondiabetic rats fed either diet displayed significantly higher lordosis and solicitation behaviors than chow-fed diabetics, and fat-fed diabetic animals displayed behavior levels intermediate to those of nondiabetic and chow-fed rats. Ten days after the induction of diabetes, the levels of hypothalamic estrogen receptors of chow-fed diabetics were significantly lower than nondiabetics with the fat-fed diabetic group showing intermediate levels. However, 70 days after streptozotocin treatment diabetic rats had significantly lower estrogen receptors than nondiabetics regardless of the diet. Treatment of long-term (70 days) diabetic rats with 1-2 U of U-100 Lente insulin for 24 hr or 7 days was ineffective in restoring the hypothalamic estrogen receptor concentrations to those of nondiabetics. Three weeks following induction of diabetes, induction of cytoplasmic progestin receptors by EB treatment was significantly impaired in diabetic animals fed either chow or high fat diet. Although the reproductive dysfunctions present in short-term diabetic female rats may be due in part to chronic fuel deprivation, it appears that the long-term maintenance of cytosol estrogen receptor level is dependent on other actions of insulin.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Progesterone-induced sequential inhibition of copulatory behavior in hysterectomized rats: relationship to neural cytoplasmic progestin receptors.

The inhibitory effects of progesterone on the copulatory behavior and on neural cytoplasmic progestin receptors were examined in ovariectomized (DV) and ovariectomized-hysterectomized (OH) rats. Ovariectomized and OH rats were given 2.0 micrograms of estradiol benzoate (EB) followed 24 hr later by 0.1, 0.5, 0.1 or 2.0 mg of progesterone (P) and were tested for lordosis 6 hr later (30 hr). Twenty four hr after the first P treatment, all animals received 0.5 mg of P and were tested again (54 hr). The initial doses of 1.0 and 2.0 mg of P significantly reduced lordosis quotients in response to the subsequent P treatment in OV animals but only the 2.0 mg dose of P effectively suppressed lordosis in OH animals. In order to determine whether the priming dose of EB influences the inhibitory effects of progesterone, OV and OH rats were injected with 1.0 microgram of EB followed by 1.0 mg of P, or 6.0 micrograms of EB followed by 2.0 mg of P and were tested for receptivity under the same schedule. Treatment with 1.0 microgram of EB permitted, and 6.0 micrograms of EB prevented sequential inhibition of sexual behavior by progesterone in both OV and OH rats. Hypothalamic cytoplasmic progestin [( 3H]R5020) receptors were then measured 48 hr after EB injection in OV or OH rats given the same treatments with EB and P. Hypothalamic progestin receptors were significantly lower in OV animals given 2.0 micrograms of EB followed by 1.0 or 2.0 mg of P than oil-treated controls, but only the 2.0 mg dose of P significantly reduced receptors in OH rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Effects of estradiol on tissue distribution of newly-synthesized fatty acids in rats and hamsters.

Estradiol treatment decreases body weight and adiposity in ovariectomized (OVX) rats and hamsters partly by increasing energy expenditure. Other manipulations which increase energy expenditure (e.g., cold exposure or overfeeding) enhance thermogenesis in brown adipose tissue (BAT) and stimulate BAT fatty acid synthesis/uptake. We examined the effect of estradiol treatment on the in vivo distribution of newly-synthesized fatty acids in OVX rats and hamsters. In both species estradiol treatment increased BAT fatty acid synthesis/uptake (incorporation of tritium from (3H)2O into lipid), consistent with the possibility that enhanced thermogenesis in BAT may contribute to estradiol-induced energy expenditure. Estradiol treatment increased BAT lipoprotein lipase (LPL) activity in hamsters, but not in rats. Thus, hamsters may utilize fatty acids synthesized in other tissues as a fuel for BAT thermogenesis, whereas rats may rely more on in situ lipogenesis. Estradiol-induced decreases in carcass adiposity (white adipose tissue mass) may be accomplished by different means in rats and hamsters. Estradiol treatment reduced white adipose tissue LPL activity and fatty acid synthesis/uptake in rats, but not in hamsters. While there are some species differences in the effects of estradiol on lipid metabolism, it appears that in both rats and hamsters estradiol acts to direct metabolic fuels (especially lipids) away from white adipose tissue storage depots and into tissues where they are oxidized (e.g., BAT). Finally, cold acclimation and estradiol had similar effects in OVX hamsters including increases in BAT fatty acid synthesis/uptake, BAT LPL activity, and energy expenditure. These findings, too, are consistent with a role for BAT in estradiol-induced thermogenesis.

Acclimatization↗
PubMed1983

Photoperiodic regulation of body mass, food intake, and reproduction in meadow voles.

Adult male voles were maintained for 10 wk in long or short photoperiods (14 or 10 h of light/day). A third group of animals housed in the long photoperiod was implanted with capsules containing melatonin. Body weight and food intake were measured weekly; various tissues were weighed and analyzed at the time of autopsy. After 10 wk, voles in the short photoperiod weighed 20% less and consumed 30% less food than those housed in the long photoperiod. Total body water and lean body mass were reduced in the short-day animals, although the size of the brown adipose tissue was not affected. White adipose tissue lipoprotein lipase (LPL) activity was markedly reduced in the short-day voles who also manifested gonadal regression and suppression of spermatogenesis. Melatonin mimicked the effects of short photoperiods on LPL activity and on lean body mass; other parameters for melatonin-treated animals were intermediate between those of untreated long- and short-day voles. We hypothesize that winter weight losses experienced by meadow voles in the field are mediated by decreases in the duration of the daily photophase and that the reduction in body mass permits overwintering voles to reduce their energy requirements and the amount of time devoted to foraging. At least part of the seasonal decline in body mass appears due to a decrease in gonadal hormone secretion.

Adipose Tissue, Brown↗
PubMed1982

Effects of photoperiod and castration on post-fast food intake and body weight gain in golden hamsters.

This experiment examined the effects of photoperiod and castration of post-food-restriction food intake and body weight gain in male golden hamsters (Mesocricetus auratus). Hamsters were ether castrated or sham-operated and housed in a 14:10 light-dark (LD) or a 8:16 LD cycle for 8 weeks. All animals were restricted to a 6 g of chow per day for 13 days and then returned to ad lib feeding. Following food restriction the hamsters gained weight rapidly without overeating. The long photoperiod (LD 14:10) increased post-restriction weight gain in castrated hamsters but decreased weight gain in gonadally intact animals. These differences in body weight gain were associated with significant group differences in feed efficiency (grams weight gain per gram eaten). The results suggest that changes in energy utilization may be more important than changes in energy intake in the adaptation of hamsters to food restriction.

Adaptation, Physiological↗
PubMed1982

Obesity without overeating in golden hamsters.

When male golden hamsters were switched from a diet of Purina rodent chow to a calorically-dense high-fat diet or were given ad lib access to a 32% sucrose solution in addition to chow, they adjusted their food intakes rapidly (within 24 hr) and did not overeat. Nevertheless, the fat-fed hamsters tripled their rate of weight gain and nearly doubled their carcass fat content after one month on the diet. Resting oxygen consumption (animals awake but quite) was significantly lower in fat-fed animals than in chow-fed controls. Sucrose feeding had no effect on food intake, body weight gain, carcass composition or oxygen consumption. Thus, whereas rats exhibit dietary obesity in spite of increases in energy expenditure (diet-induced thermogenesis), fat-fed hamsters seem to become obese because of decreases in energy expenditure. However, although actual energy expenditure is reduced, fat-fed hamsters exhibit an enhanced thermogenic capacity. Interscapular brown adipose tissue mass, protein content, and DNA content as well as norepinephrine-stimulated oxygen consumption were all significantly elevated in fat-fed hamsters. The significance of these concurrent diet-induced decreases in energy expenditure and increases in thermogenic capacity is not clear, but they could be of some value in preparing the hamster for winter.

Adipose Tissue↗
PubMed1982

Metabolic and physiologic effects of a hunger-inducing injection of insulin.

Rats injected subcutaneously with 5 U/kg of regular insulin increased food intake above control levels in a 2 hr test and showed a median latency to eat of 59 min. One week later, rats were injected again with saline or insulin (5 U/kg), deprived of food and killed 60 +/- 10 min later. Insulin treatment produced a marked reduction in plasma glucose, plasma ketone bodies and liver glycogen, as well as a marked acceleration of gastric emptying. The results indicate that a variety of changes in peripheral metabolism and physiology may underlie the increase in food intake observed after insulin injection and that it is premature to ascribe the hunger-inducing effect of insulin treatment solely to a decline in blood glucose.

Animals↗
PubMed1981

Effects of androgens on dietary self-selection and carcass composition in male rats.

The aromatizable androgen testosterone propionate (TP; .2 mg/day) increased protein and carbohydrate intake and stimulated body weight gain in gonadectomized (Gdx) male rats. A higher dose of TP (2.0 mg/day) increased protein, but not carbohydrate, intake and was less effective in stimulating body weight gain than the lower dose of TP. Postmortem carcass analyses revealed that the elevated protein intake of both TP-tested groups was associated with increased carcass protein content. The decreased weight of rats treated with the high dose of TP was due to a reduction in body fat content. The nonaromatizable androgen 5 alpha-dihydrotestosterone propionate (DHTP; .2 or 2.0 mg/day) also increased protein (but not carbohydrate) intake and body weight gain in Gdx male rats, but it did not alter carcass composition. Unlike TP, the two doses of DHTP were equally effective, but neither dose of DHTP was as effective as the low dose of TP in stimulating protein and carbohydrate intake and body weight gain. The results of these experiments suggest that (a) androgens can increase selection of dietary protein whether or not they exert significant protein anabolic effects, (b) the 5 alpha-reduced product of testosterone, 5 alpha-dihydrotestosterone, is not the major metabolite responsible for the increases in protein and caloric intake and in body weight caused by TP, and (c) the decreases in carbohydrate intake and adiposity in rats treated with the high dose of TP may be mediated by aromatized (estrogenic) metabolites of the androgen.

Animals↗
PubMed1981

In vivo cell nuclear binding of 17 beta-[3H]estradiol in rat adipose tissues.

Rat adipose tissues contain high-affinity, hormone-specific cytoplasmic estrogen receptors. If adipose tissues are actually estrogen target tissues, then it should be possible to demonstrate in vivo binding and retention of 17 beta-[2H]estradiol in adipose tissue cell nuclei, the putative subcellular site of steroid action. Gonadectomized rats were given an intravenous injection of 40 microCi (0.11 microgram) 17 beta-[2,4,6,7-3H]estradiol. Animals were then killed, and cell nuclei were isolated from hypothalamus and various fat pads. Cell nuclear levels of radioactivity peaked at 1 h in both hypothalamus and parametrial adipose tissue, but the peak cell nuclear concentration in the fat pad was more than twice that in hypothalamus. At 1 h, 89% of the adipose tissue nuclear radioactivity migrated with 17 beta-estradiol on thin-layer plates. Radioactivity was retained in cell nuclei for more than 6 h in both tissues. This cell nuclear binding was estrogen specific. Pretreatment with radioinert estrogens (17 beta-estradiol or R 2858) abolished cell nuclear 17 beta-[3H]estradiol uptake, but other steroids (progesterone, corticosterone, and 5 alpha-dihydrotestosterone) were without effect. Cell nuclear binding was found in all fat pads studied in both males and females. Levels were highest in parametrial (females) and epididymal (males) fat pads, the depots with the highest concentration of cytoplasmic estrogen receptor. There were no sex differences in cell nuclear binding. Taken together these findings provide strong support for the contention that 17 beta-estradiol could affect lipid metabolism and body fat content in part by direct action on adipose tissues.

Adipose Tissue↗
PubMed1981

Food intake, body weight, and adiposity in female rats: actions and interactions of progestins and antiestrogens.

A series of experiments examined the effects of two progestins, progesterone and R 5020, and two nonsteroidal antiestrogens, nafoxidine and MER-25, on body weight and composition in female rats. Both progesterone and R 5020 increased food intake, body weight, and carcass adiposity in ovariectomized (OVX) rats treated with estradiol benzoate (EB), but neither progestin had any effect on these measures in OVX rats not treated with EB. R 5020 was substantially more effective than progesterone on all end points. Nafoxidine and MER-25 mimicked the actions of estradiol and decreased adipose tissue lipoprotein lipase (LPL) activity by 75-80%. For adipose tissue LPL activity, both nafoxidine and MER-25 were full estrogen agonists and without antiestrogenic activity. Nafoxidine also mimicked the effects of EB by reducing food intake, body weight, and carcass adiposity in OVX rats. In contrast, nafoxidine antagonized the induction of cytoplasmic progestin ([3H]R 5020) binding sites by EB in parametrial adipose tissue of OVX rats. In nafoxidine-treated OVX rats, concurrent progesterone administration had no effect on adipose tissue LPL activity, but progesterone did increase food intake, body weight, and carcass fat content. Some physiological mechanisms by which gonadal steroids may act to influence eating and adiposity are discussed.

Adipose Tissue↗
PubMed1981

Effects of estradiol and progesterone on food intake, body weight, and carcass adiposity in weanling rats.

The effects of estradiol and progesterone on food intake, body weight, carcass adiposity, and adipose tissue lipoprotein lipase (LPL) activity were investigated in weanling female rats. Treatment with estradiol benzoate (EB) reduced body weight gain in ovariectomized (OVX) weanlings as it does in adults. However, other responses to EB were attenuated or absent in weanlings. EB treatment did not reduce food intake, carcass adiposity, or adipose tissue LPL activity. This impaired responsiveness to EB may be due to decreased levels of cytoplasmic estrogen receptors in liver and adipose tissue (but not hypothalamus) in weanlings. On the other hand, responsiveness to progesterone was adultlike in weanlings. Treatment of OVX, EB-primed weanlings with progesterone increased food intake, body weight gain, and carcass adiposity. This adultlike responsiveness to progesterone was associated with adultlike levels of adipose tissue progestin receptors. However, progesterone treatment did not increase adipose tissue LPL activity in weanlings, indicating that changes in LPL activity are not necessary for progesterone-induced obesity.

Adipose Tissue↗
PubMed1981

Deficits in pituitary and brain cell nuclear retention of (3H)Estradiol in diabetic rats deprived of insulin: time course and metabolic correlates.

Withdrawal of exogenous insulin for 24 h in ovariectomized, streptozotocin-diabetic rats significantly impairs estradiol uptake in whole homogenate fractions of hypothalamus-preoptic area and pituitary gland. Significant reductions in cell nuclear fractions from the same tissues are seen after 36 h of insulin deprivation. Subsequent reinstatement of insulin treatment does not yield full recovery of estradiol uptake after 24 h of insulin replacement. Fat content of the diet has no effect on brain or pituitary estradiol uptake in diabetic animals deprived of insulin for 36 h. Circulating levels of triglycerides, ketones, glucose, glycerol and free fatty acids were found to predict uptake levels to a significant extent, but no single metabolite is reliably predictive across tissues. These data demonstrate that insulin-dependent changes in brain and pituitary uptake of estradiol in rats are slow to develop, and they support the hypothesis that at least some of the reproductive dysfunctions observed in diabetic rats may be the result of impaired cell nuclear estradiol binding in hypothalamus and pituitary.

Animals↗
PubMed1981

Estrous behavior and pituitary and brain cell nuclear retention of [3H]estradiol in chronically insulin-deficient female rats.

Chronic insulin deficiency, produced by administration of 60 mg/kg streptozotocin, leads to reduced estrous behavior and lower estradiol uptake in both whole homogenate and cell nuclear fractions of hypothalamus-preoptic area and pituitary gland in ovariectomized rats. High dietary fat intake produces an ameliorative effect on both lordosis behavior and estradiol uptake, relative to animals fed a standard, carbohydrate-rich diet. Plasma glucose levels are significantly correlated with estradiol uptake levels in brain and pituitary, and with plasma radioactivity levels. The data support the hypothesis that some of the reproductive dysfunctions manifest in female diabetic rats are the result of alterations in nuclear binding of estradiol by central nervous tissue, and that chronic fuel deprivation may represent an important correlate of disruptions in normal steroid action among diabetics.

Animals↗