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  • American Physiological Society  (40)
  • 1
    Online Resource
    Online Resource
    American Physiological Society ; 1994
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 266, No. 6 ( 1994-06-01), p. R1765-R1770
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 266, No. 6 ( 1994-06-01), p. R1765-R1770
    Abstract: Intracerebroventricular injection of neuropeptide Y (NPY) has two effects on energy metabolism in addition to increased feeding: decreased brown fat thermogenesis and increased white fat lipoprotein lipase (LPL) enzymatic activity. We hypothesized that the paraventricular nucleus (PVN) of the hypothalamus is the controlling neural site for these responses. We further hypothesized that NPY stimulation at PVN would reduce gene expression for the critical brown fat thermogenic protein, uncoupling protein (UCP), and increase gene expression for the key white fat storage enzyme, LPL. In the first experiment, three groups of rats received injections every 6 h for 24 h (5 injections total) into the PVN:1) NPY (1 micrograms/1 microliters injection) and ad libitum food; 2) NPY (1 micrograms/1 microliters injection) and food restricted to control intake; 3) saline injection (1 microliter) and ad libitum food. Both NPY-treated groups showed significant reductions (P 〈 0.05) in brown fat UCP mRNA levels and marked stimulation of LPL mRNA levels relative to controls. In the second experiment, four groups of seven rats had NPY injected into the PVN:0 (vehicle control); 0.1 microgram; 0.5 microgram; and 1 microgram. Injections were made every 6 h for 24 h. There was a dose-related reduction in UCP mRNA produced by the NPY treatment. NPY treatment increased LPL mRNA, but a smooth dosing effect was not evident. The observation that NPY in the PVN can coordinate more than one component of energy metabolism is significant when considered with many reports of responsiveness of NPY activity in the arcuate nucleus-PVN neural circuit to perturbations of energy balance such as fasting and feeding, diabetes, and genetic obesity.(ABSTRACT TRUNCATED AT 250 WORDS)
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1994
    detail.hit.zdb_id: 1477297-8
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    American Physiological Society ; 1987
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 252, No. 1 ( 1987-01-01), p. R160-R165
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 252, No. 1 ( 1987-01-01), p. R160-R165
    Abstract: Despite long-standing observations of a whole-body thermogenic effect of glucagon, the role of glucagon in activating thermogenesis in brown adipose tissue has not often been studied. We investigated the ability of administered glucagon to produce alterations in brown adipose tissue similar to changes produced by accepted stimuli of brown fat activity: cold, norepinephrine, and overfeeding. Eighteen days of glucagon injections (1 mg/kg) to male Sprague-Dawley rats produced, relative to saline-injected controls, decreases in feed efficiency and increases in brown adipose tissue weight, protein content, DNA content, and mitochondrial mass as reflected in cytochrome oxidase activity. The observed changes were similar, though of lesser magnitude, to changes produced in these same parameters induced by administration of norepinephrine (250 micrograms/kg) for a positive control group. Four days of glucagon administration (1 mg/kg) produced increases in specific activity of cytochrome oxidase and lipoprotein lipase. After 8 days of glucagon administration, changes in whole-pad activity similar to those seen with 18 days of administration were present. Glucagon also increased whole-pad lipoprotein lipase activity after 4 and 8 days. Surgically denervated interscapular brown adipose tissue retained its ability to respond to exogenous glucagon, though the magnitude of the response was diminished. Guanosine 5'-diphosphate (GDP) binding to brown adipose tissue mitochondria was measured as an assessment of functional state after 5 days of glucagon (1 mg/kg). There was an increase in GDP binding relative to controls whether expressed as picomoles per milligram mitochondrial protein or nanomoles per pad.(ABSTRACT TRUNCATED AT 250 WORDS)
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1987
    detail.hit.zdb_id: 1477297-8
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    American Physiological Society ; 1996
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 271, No. 1 ( 1996-07-01), p. R217-R221
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 271, No. 1 ( 1996-07-01), p. R217-R221
    Abstract: Modulation of feeding behavior by neuropeptide Y (NPY) and opioids is well established, but the possibility that these neural influences provoke specific appetites, NPY for carbohydrate and opioids for fat, has also been considered. In other studies, intake of standard chow after NPY stimulation can be blocked by naloxone, indicating an interaction between these systems in the regulation of feeding. The present experiments examined the nature of NPY-opioid interactions in diet selection. Rats were administered NPY and naloxone concurrently, then chose between high-fat and high-carbohydrate diets. Subcutaneous administration of naloxone (0.01-0.3 mg/kg) potently reduced intake of the preferred diet, but not the nonpreferred diet. A similar pattern of selection was seen in a separate experiment where the same doses of naloxone were administered after 24-h food deprivation. These data support the idea that the opioid system mediates the “rewarding” aspects of feeding.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1996
    detail.hit.zdb_id: 1477297-8
    SSG: 12
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  • 4
    Online Resource
    Online Resource
    American Physiological Society ; 1991
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 261, No. 2 ( 1991-08-01), p. R501-R507
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 261, No. 2 ( 1991-08-01), p. R501-R507
    Abstract: Our aims were to further characterize the stimulatory effect of glucagon on brown fat and to test the hypothesis that physiological levels of hyperglucagonemia would stimulate brown fat thermogenesis. In the first set of experiments, glucagon (1 mg/kg sc twice daily) or vehicle control was administered three times in 26 h. This large dose of glucagon produced increases in GDP binding to brown fat mitochondria. In addition, Scatchard analysis indicated a glucagon-induced increase in number of GDP binding sites without evidence for alteration in binding site affinity. No consistent increase in brown fat mitochondrial GDP binding was produced 2 h after a single injection of glucagon (1 mg/kg). In the second set of experiments, glucagon was administered intraperitoneally by constant osmotic minipump infusion. Glucagon in a dose of 150 micrograms.kg-1.day-1 for 5 days produced significant increases in GDP binding to brown fat mitochondria, whereas glucagon serum levels were increased but stayed within the usual physiological range. A larger dose of glucagon administered by constant infusion virtually eliminated body weight gain over 7 days while significantly increasing nucleotide binding (GDP) to brown fat mitochondria. An important role for glucagon in thermogenic regulation is suggested.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1991
    detail.hit.zdb_id: 1477297-8
    SSG: 12
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  • 5
    Online Resource
    Online Resource
    American Physiological Society ; 1986
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 251, No. 6 ( 1986-12-01), p. R1109-R1117
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 251, No. 6 ( 1986-12-01), p. R1109-R1117
    Abstract: The role of insulin and brown adipose tissue (BAT) thermogenesis in metabolic efficiency (ME, the efficiency of body wt gain) was examined in rats with varied basal insulin status. Long-lasting insulin was administered using a protocol that did not alter food intake, yet increased ME in both groups. Half the rats were fed sucrose to stimulate BAT growth and thermogenesis. Insulin overrode the exaggerated decrease in ME in sucrose-fed diabetics, with only partial attenuation in controls. Interscapular BAT (IBAT) lipoprotein lipase activity was decreased in diabetic rats, restored by insulin treatment, and not affected in controls. Sucrose-fed diabetics and controls had their IBAT sham or bilaterally surgically denervated. Insulin decreased the thermogenic potential of BAT [cytochrome oxidase activity (COA)] in intact controls and diabetics; in the latter, insulin restored COA independent of BAT innervation. We conclude that insulin can increase ME without an associated increase in energy intake, regardless of basal insulin status, both insulin deficiency and excess decrease BAT thermogenic potential (COA), and hyperinsulinemia-induced increases in ME may result from decreased BAT mitochondrial proliferation.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1986
    detail.hit.zdb_id: 1477297-8
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    American Physiological Society ; 1986
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 251, No. 6 ( 1986-12-01), p. R1118-R1125
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 251, No. 6 ( 1986-12-01), p. R1118-R1125
    Abstract: The role of insulin in metabolic efficiency (ME, i.e., efficiency of body wt gain) was examined under conditions of maximal energy expenditure in control and diabetic rats. Long-lasting insulin was administered using a protocol that did not affect food intake and increased ME in both groups. Half the animals were injected chronically with norepinephrine (NE). NE alone in controls decreased body weight and ME and increased brown adipose tissue (BAT) growth, thermogenic potential [cytochrome c oxidase activity (COA)], and lipoprotein lipases (LPL) activity; however, in diabetics, body weight, ME, and food intake all decreased and only BAT LPL activity and DNA content increased. The combination of NE and insulin increased BAT protein and COA in diabetics; in controls, all BAT measures were further increased and ME was intermediate to that of either treatment alone. Cold exposure decreased body weight and ME, increased food intake and qualitatively produced similar increases in BAT growth, COA, and LPL activity in both controls and diabetics. In diabetics, combined cold exposure and insulin did not affect the increase in BAT growth or LPL activity resulting from either treatment alone, but in controls this combination decreased BAT growth and COA. It is concluded that, even under conditions of maximal energy expenditure, both extremes of basal insulin status result in decreased BAT growth and thermogenic potential, but have opposite effects on ME.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1986
    detail.hit.zdb_id: 1477297-8
    SSG: 12
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  • 7
    Online Resource
    Online Resource
    American Physiological Society ; 1995
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 269, No. 2 ( 1995-08-01), p. R357-R364
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 269, No. 2 ( 1995-08-01), p. R357-R364
    Abstract: We were interested in determining whether season affects the ability of cold exposure to increase brown adipose tissue (BAT) thermogenic function in 13-lined ground squirrels after acute and chronic cold (4 degrees C) exposure. Tissues were collected from animals in April and September after cold exposure for 12, 24, or 48 h. Animals chronically exposed to the cold (10 days) were killed in early May and mid-August. We found that mitochondrial uncoupling protein (UCP) concentrations varied seasonally, with concentrations in control animals (at 23 degrees C) higher in late summer (mid-August and September) than in the spring (April and early May). Cold exposure in late summer did not induce further increases in UCP concentrations. In contrast, when animals were cold exposed in the spring, UCP concentrations and total UCP increased. Surprisingly, 10 days at 4 degrees C did not cause a greater increase in UCP concentrations than did 24 h at 4 degrees C. Chronic cold exposure increased the UCP mRNA-to-beta-actin mRNA ratio 48% in May, whereas a fivefold increase occurred in August. GDP binding was increased after 12 h at 4 degrees C in April; in contrast, animals attempted to hibernate when placed in the cold in September, and no increase in GDP binding was observed. Chronic cold exposure caused GDP binding to increase at both times. These results indicate that mitochondrial UCP concentrations are seasonally regulated in the 13-lined ground squirrel.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1995
    detail.hit.zdb_id: 1477297-8
    SSG: 12
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  • 8
    Online Resource
    Online Resource
    American Physiological Society ; 1993
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 264, No. 1 ( 1993-01-01), p. R16-R21
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 264, No. 1 ( 1993-01-01), p. R16-R21
    Abstract: The effect of lactation on brown adipose tissue (BAT) thermogenic activity and capacity as well as on uncoupling protein (UCP) gene expression has been studied in the 13-lined ground squirrel. Lactating animals were studied after approximately 21 days of lactation. Parameters of thermogenesis were also studied in a group of postpregnant animals from which litters had been removed at 1-2 days postpartum. A group of animals that did not bear litters served as nonpregnant controls. BAT pad weights, protein concentration, and mitochondrial mass were all significantly decreased relative to nonpregnant controls and postpregnant animals. Specific binding of GDP and total GDP bound were significantly decreased in lactating animals relative to both nonpregnant and postpregnant animals. Scatchard analysis of GDP binding indicated that binding affinity (Kd) was unaffected by treatment. UCP concentrations were reduced by 26% during lactation, whereas total UCP content was reduced by 70%. A 3-wk period after pup removal was sufficient for UCP concentrations to return to nonpregnant levels, although total UCP content remained reduced. The changes in UCP concentrations were accompanied by parallel alterations of gene expression. UCP mRNA-to-beta-actin mRNA ratios during lactation were 30% of the levels found in nonpregnant controls and postpregnant animals. The results presented here clearly indicate that BAT activity and capacity are suppressed during lactation in the 13-lined ground squirrel.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1993
    detail.hit.zdb_id: 1477297-8
    SSG: 12
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  • 9
    Online Resource
    Online Resource
    American Physiological Society ; 1989
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 257, No. 3 ( 1989-09-01), p. R536-R541
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 257, No. 3 ( 1989-09-01), p. R536-R541
    Abstract: The effect of hibernation and arousal on brown adipose tissue (BAT) cytochrome-c oxidase activity and GDP binding, as well-circulating metabolites, have been studied in the 13-lined ground squirrel. Control animals (warm adapted) were housed continuously at 23 degrees C, while the remaining animals were transferred into a cold room (4 degrees C) for 8 days to induce hibernation. Hibernating animals were killed while deeply hibernating. Aroused animals were manually stimulated to induce arousal or had spontaneously aroused on the day of the experiment. BAT weight as well as mitochondrial mass were increased in both groups of cold-adapted animals, relative to controls. A substantial increase in GDP binding, however, was seen only in aroused animals, an observation confirmed by Scatchard analysis. Arousal was also accompanied by marked alterations in the levels of several circulating metabolites. Plasma free fatty acids declined by approximately 20% despite a three- to fourfold increase in plasma glycerol concentrations. Plasma lactate levels increased eightfold, while concentrations of beta-hydroxybutyrate were five times lower during arousal than hibernation. These data are consistent with the idea that the oxidation of free fatty acids, glucose, and ketone bodies are all increased during arousal. In conclusion, we have found that cold adaptation and subsequent hibernation increases BAT thermogenic capacity in the 13-lined ground squirrel. However, this increase in thermogenic potential is not manifested as a substantial increase in BAT thermogenic activity until arousal is initiated.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1989
    detail.hit.zdb_id: 1477297-8
    SSG: 12
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  • 10
    Online Resource
    Online Resource
    American Physiological Society ; 1994
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 266, No. 5 ( 1994-05-01), p. R1578-R1583
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 266, No. 5 ( 1994-05-01), p. R1578-R1583
    Abstract: We measured the influence of diet composition on hypothalamic neuropeptide Y (NPY) message and brown fat uncoupling protein (UCP) mRNA using different diets. Sprague-Dawley rats ate ad libitum either chow, a high-carbohydrate (HC), an intermediate-carbohydrate (IHC), a high-fat (HF), or an intermediate-fat (IHF) diet, all with equal protein content (g/kcal). The HF and IHF groups ate less food mass and, except for HC, all groups consumed similar kilocalories during the study. After 1 wk, we killed the animals and extracted total RNA from arcuate nucleus, cortex, and brown adipose tissue (BAT). Arcuate NPY mRNA in the HF group was significantly (P 〈 0.001) lower than in the HC and chow group. There were no differences between groups in NPY message in cortex or NPY protein in the paraventricular nucleus. BAT UCP message levels were significantly higher (P = 0.001) in the HF group. Thus HF compared with HC and chow diet reduces expression of NPY mRNA in hypothalamic nuclei and increases expression of BAT UCP message.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1994
    detail.hit.zdb_id: 1477297-8
    SSG: 12
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