Effects of caffeine on energy metabolism, heart rate, and methylxanthine metabolism in lean and obese women

1995 ◽  
Vol 269 (4) ◽  
pp. E671-E678 ◽  
Author(s):  
D. Bracco ◽  
J. M. Ferrarra ◽  
M. J. Arnaud ◽  
E. Jequier ◽  
Y. Schutz
Keyword(s):  
Heart Rate ◽  
Energy Metabolism ◽  
Lipid Oxidation ◽  
Substrate Oxidation ◽  
The Other ◽  
Obese Women ◽  
Concomitant Increase ◽  
Decaffeinated Coffee ◽  
Caffeinated Coffee ◽  
Stimulation Of

The magnitude of coffee-induced thermogenesis and the influence of coffee ingestion on substrate oxidation were investigated in 10 lean and 10 obese women, over two 24-h periods in a respiratory chamber. On one occasion the subjects consumed caffeinated coffee and on the other occasion, decaffeinated coffee. The magnitude of thermogenesis was smaller in obese (4.9 +/- 2.0%) than in lean subjects (7.6 +/- 1.3%). The thermogeneic response to caffeine was prolonged during the night in lean women only. The coffee-induced stimulation of energy expenditure was mediated by a concomitant increase in lipid and carbohydrate oxidation. During the next day, in postabsorptive basal conditions, the thermogenic effect of coffee had vanished, but a significant increase in lipid oxidation was observed in both groups. The magnitude of this effect was, however, blunted in obese women (lipid oxidation increased by 29 and 10% in lean and obese women, respectively). Caffeine increased urinary epinephrine excretion. Whereas urinary caffeine excretion was similar in both groups, obese women excreted more theobromine, theophylline, and paraxanthine than lean women. Despite the high levels of urinary methylxanthine excretion, thermogenesis and lipid oxidation were less stimulated in obese than in lean subjects.

scholarly journals Preliminary findings on the role of PLIN1 polymorphisms on body composition and energy metabolism response to energy restriction in obese women

2011 ◽  
Vol 106 (4) ◽  
pp. 486-490 ◽  
Author(s):  
J. R. Ruiz ◽  
E. Larrarte ◽  
J. Margareto ◽  
R. Ares ◽  
P. Alkorta ◽  
...  
Keyword(s):  
Body Composition ◽  
Energy Metabolism ◽  
Waist Circumference ◽  
Lipid Oxidation ◽  
Body Fat ◽  
Oxidation Rate ◽  
Energy Restriction ◽  
Obese Women ◽  
Restricted Diet ◽  
Induced Changes

The aim of the present study was to investigate the association of PLIN1 11482G>A (rs894160) and PLIN1 13041A>G (rs2304795) polymorphisms with body composition, energy and substrate metabolism, and the metabolic response to a 12-week energy-restricted diet in obese women. The study comprised a total of seventy-eight obese (BMI 34·0 (sd 2·8) kg/m2) women (age 36·7 (sd 7) years). We measured weight, height and waist circumference before and after a 12-week controlled energy-restricted diet intervention. Body fat mass and lean mass were measured by dual-energy X-ray absorptiometry. RMR and lipid oxidation rate were measured by indirect calorimetry. We also analysed fasting plasma glucose, insulin, cholesterol and leptin. Women carrying the 11482A allele had a lower reduction in waist circumference than non-A allele carriers (3·2 (sd 0·5) v. 4·6 (sd 0·6) %, respectively, P = 0·047; P for gene–diet interaction = 0·064). Moreover, women with the 11482A allele had a higher decrease in lipid oxidation rate than non-A allele carriers (58·9 (sd 6·7) v. 31·3 (sd 8·2) %, respectively, P = 0·012; P for gene–diet interaction = 0·004). There was no interaction effect between the 13041A>G polymorphism and diet-induced changes on the outcome variables (all P>0·1). These results confirm and extend previous findings suggesting that the PLIN1 11482G>A polymorphism plays a modulating role on diet-induced changes in body fat and energy metabolism in obese women.

Neopterin and 7,8-dihydroneopterin are generated within atherosclerotic plaques

Pteridines ◽  
2015 ◽  
Vol 26 (3) ◽  
pp. 93-103 ◽  
Author(s):  
Tejraj Janmale ◽  
Rebecca Genet ◽  
Elizabeth Crone ◽  
Elizabeth Flavall ◽  
Carol Firth ◽  
...  
Keyword(s):  
Lipid Oxidation ◽  
Scavenger Receptor ◽  
Lipid Peroxides ◽  
The Other ◽  
Atherosclerotic Plaques ◽  
Macrophage Cell ◽  
Cd36 Expression ◽  
The Media ◽  
Γ Interferon ◽  
Stimulation Of

AbstractPlasma neopterin correlates with the level of cardiovascular disease. Neopterin is the oxidation product of 7,8-dihydroneopterin, which is released by γ-interferon-stimulated macrophages. 7,8-Dihydroneopterin is a potent antioxidant, which inhibits lipid oxidation, macrophage cell death and scavenger receptor CD36 expression. The concentration of neopterin within atherosclerotic plaques was measured in tissue removed from carotid and femoral arteries. The excised plaques were cut into 3-mm-thick sections, and each section was analysed for neopterin, total neopterin, cholesterol, lipid peroxides, α-tocopherol and protein-bound 3,4-dihydroxyphenylalanine. Selected plaques were placed in tissue culture, and the media was analysed for 7,8-dihydroneopterin and neopterin release. Total neopterin levels ranged from 14 to 18.8 nmol/g of tissue. Large ranges of values were seen both within the same plaque and between plaques. No correlation between neopterin and any of the other analytes was observed, nor was there any significant trend in levels along the length of the plaques. γ-Interferon stimulation of cultured plaque generated total neopterin concentrations from 1 to 4 nmol/(g 24 h). The level of 7,8-dihydroneopterin generated within the plaque was within the range that inhibits lipid oxidation. The data show that atherosclerotic plaques are extremely dynamic in biochemistry and are the likely source of the plasma 7,8-dihydroneopterin and neopterin.

Prolonged Daytime Exercise Repeated Over 4 Days Increases Sleeping Heart Rate and Metabolic Rate

2003 ◽  
Vol 28 (4) ◽  
pp. 616-629 ◽  
Author(s):  
Isabelle Mischler ◽  
Michel Vermorel ◽  
Christophe Montaurier ◽  
Rémi Mounier ◽  
Vincent Pialoux ◽  
...  
Keyword(s):  
Heart Rate ◽  
Metabolic Rate ◽  
Lipid Oxidation ◽  
Prolonged Exercise ◽  
Cycle Ergometer ◽  
Moderate Intensity ◽  
Significant Relationships ◽  
Exercise Period ◽  
Sympathetic Nervous ◽  
Stimulation Of

The aim of this study was to determine the influence of prolonged exercise repeated for 4 days on sleeping heart rate (SHR) and metabolic rate (SMR). Eleven young untrained men exercised at moderate intensity 5 hrs daily for 4 days, alternately on a cycle ergometer (57.0 ± 1.3% [Formula: see text]) and a treadmill (64.7 ± 1.6% [Formula: see text]). They spent the night prior to the exercise period (control, C) and the 4 nights following exercise days (N1 to N4) in room calorimeters for the measurement of SHR, SMR, and respiratory quotient (RQ) from midnight until 6 a.m. Every morning, before the exercise bouts, plasma-free epinephrine (E) and norepinephrine (NE) levels were measured. After exercise, all SHR values were significantly higher than at C level (52 ± 1 bpm, p < 0.001) and the highest value was observed on N2 (61 ± 2 bpm). SMR increased by 11.2 ± 1.5% from C to N1, p < 0.001, and then plateaued up to N4, whereas RQ decreased from C (0.833 ± 0.009) to N2 (0.798 ± 0.005) and then plateaued. Plasma NE levels were higher the morning after each day of exercise and peaked on N2, whereas no significant variations were found for E. Variations of SHR between C and N2, and N3 and N4 were correlated with changes of SMR. No significant relationships were found between morning plasma NE, and either SMR or SHR variations. To conclude, prolonged exercise repeated for 4 days was associated with increases in SHR and SMR during the night following each day of exercise concomitantly with an enhanced lipid oxidation. The sustained stimulation of the sympathetic nervous system may be partly responsible for these effects. Key words: lipid oxidation, catecholamines, room calorimeter, endurance trial

Effects of Caffeine on the Trigeminal Blink Reflex

2005 ◽  
Vol 100 (2) ◽  
pp. 493-496 ◽  
Author(s):  
Edward J. Schicatano
Keyword(s):  
Trigeminal Nerve ◽  
Acoustic Startle ◽  
Startle Reflex ◽  
Blink Reflex ◽  
Psychomotor Effects ◽  
Brainstem Reflex ◽  
Decaffeinated Coffee ◽  
Reflex Blinks ◽  
Caffeinated Coffee ◽  
Stimulation Of

The acoustic startle and trigeminal blink reflexes share the same motor output. Since caffeine has been shown to augment the startle reflex, it was proposed that caffeine would also increase the trigeminal blink reflex. In 6 humans, the effects of caffeine (100 mg) on the trigeminal blink reflex were investigated. Reflex blinks were elicited by stimulation of the supraorbital branch of the trigeminal nerve. Following ingestion of caffeinated coffee, reflex blinks increased in amplitude and duration and occurred at a shorter latency than reflex blinks following ingestion of decaffeinated coffee. Since the blink reflex is a brainstem reflex, these results suggest that the psychomotor effects of caffeine facilitate brainstem processing.

THE EFFECT OF IODINE DEFICIENCY AND SUPPRESSION OF TSH SECRETION ON RADIOIODINE LABELLED THYROXINE AND TRIIODOTHYRONINE IN THE THYROID OF RATS

1971 ◽  
Vol 68 (2) ◽  
pp. 377-386 ◽  
Author(s):  
D. Emrich ◽  
A. v. zur Mühlen ◽  
G. Burmeister ◽  
H.-D. Zimmermann ◽  
R. Beckmann
Keyword(s):  
Heart Rate ◽  
Thyroid Gland ◽  
Iodine Deficiency ◽  
Iodine Concentration ◽  
Conversion Ratio ◽  
The Other ◽  
Normal Range ◽  
Tsh Secretion ◽  
Tsh Stimulation ◽  
Stimulation Of

ABSTRACT It has been suggested that TSH stimulation of the thyroid gland is accompanied by an alteration in the ratio of newly synthesized thyroxine (*T4)1)/triiodothyronine (*T3) in favour of *T3. Evidence in support of this hypothesis is provided here by the finding that suppression of TSH secretion in rats alters this ratio in the other direction, i. e. in favour of *T4. Thus, endogenous TSH stimulation was increased for 4 weeks by iodine deficiency. Its suppression was performed by the administration of T3, using a dose of 0.05-0.25 μg/100 g body weight which was injected subcutaneously every 12 hours for three days. The effect of TSH stimulation and suppression could be assessed from the following parameters: thyroid weight and histology, thyroid 131I uptake, 131I conversion ratio, hormonal iodine concentration, and TSH level in the plasma. After iodine deficiency the ratio of *T4/*T3 in the thyroid gland changed in favour of *T3. This may compensate for the iodine deficiency, since the oxygen consumption and the heart rate of the animals remained in the normal range. After suppression the ratio of *T4/*T3 changed in the opposite direction, i. e. in favour of *T4. The extent of the suppression of *T4 and *T3 was dependent on the suppression dose used.

scholarly journals Effects of red pepper added to high-fat and high-carbohydrate meals on energy metabolism and substrate utilization in Japanese women

1998 ◽  
Vol 80 (6) ◽  
pp. 503-510 ◽  
Author(s):  
Mayumi Yoshioka ◽  
Sylvie St-Pierre ◽  
Masashige Suzuki ◽  
Angelo Tremblay
Keyword(s):  
Energy Metabolism ◽  
Energy Expenditure ◽  
Lipid Oxidation ◽  
Carbohydrate Oxidation ◽  
The Other ◽  
Red Pepper ◽  
High Fat ◽  
High Carbohydrate ◽  
Japanese Female ◽  
Diet Induced Thermogenesis

The effects of dietary red pepper added to high-fat (HF) and high-carbohydrate (HC) meals on energy metabolism were examined in thirteen Japanese female subjects. After ingesting a standardized dinner on the previous evening, the subjects took an experimental breakfast (1883 kJ) under the following four conditions: HF meal, HF and red-pepper (10 g) meal, HC meal, or HC and red-pepper meal. Palatability of the experimental meals was measured immediately after the meals. Expired air was collected before and for 210 min after the meal to determine energy expenditure and macronutrient oxidation. Diet-induced thermogenesis was significantly higher after the HC meals than after the HF meals. Lipid oxidation was significantly lower and carbohydrate oxidation was significantly higher after the HC meals than after the HF meals. Addition of red pepper to the experimental meals significantly increased diet-induced thermogenesis and lipid oxidation, particularly after the HF meal. On the other hand, carbohydrate oxidation was significantly decreased by the addition of red pepper to the experimental meals. Addition of red pepper to the HC meal increased the perceived oiliness of the meal to the same level as that of the HF meals. These results indicate that red pepper increases diet-induced thermogenesis and lipid oxidation. This increase in lipid oxidation is mainly observed when foods have a HF content whereas the increase in the perceived oiliness of the meal was found under the HC meal conditions.

Conversion and release of an intermediate in vasopressin–neurophysin biosynthesis in the guinea-pig

1984 ◽  
Vol 103 (3) ◽  
pp. 347-354 ◽  
Author(s):  
P. M. Jones ◽  
T. Saermark ◽  
I. C. A. F. Robinson
Keyword(s):  
Guinea Pig ◽  
The Other ◽  
Concomitant Increase ◽  
Temperature Dependent ◽  
Neural Lobe ◽  
In Vivo Labelling ◽  
Processed Form ◽  
Stimulation Of

ABSTRACT Guinea-pig neural lobes contain appreciable amounts of neurophysin with a glycopeptide extension (NPGP) which may represent a partially processed form of the arginine vasopressin (AVP) precursor. We have now studied the turnover and release of the NPGP component using a combination of in-vivo radiolabel incorporation and high pressure liquid chromatography. Measurement of the neural lobe content of 35S-labelled peptides at various times after hypothalamic injection of [35S]cysteine demonstrated that the oxytocin-related products accumulated more rapidly than the AVP-related products. The relative amounts of [35S]cysteine incorporated into NPGP and the AVP-related neurophysin (NPavp) changed markedly with time after in-vivo labelling. In-vitro incubation of neurosecretory granules prepared from neural lobes 4 h after radiolabel injection produced a time- and temperature-dependent conversion of NPGP to NPavp. Incubation at 37 °C for 4 h produced a 30% decrease in [35S]NPGP with a concomitant increase in [35S]NPavp, whilst there were no changes in the other 35S-labelled components. In-vitro stimulation of radiolabelled neural lobes by 56 mm-K+ evoked a Ca++-dependent release of NPGP as well as the other expected neurosecretory components, and the amount of NPGP released reflected its neural lobe content. We conclude that the NPGP component found in guinea-pig neural lobes is a biosynthetic intermediate, most of which is further processed to NPavp. However, some NPGP may also be secreted from the neural lobe in an intact form. J. Endocr. (1984) 103, 347–354

EFFECT OF ACTINOMYCIN D ON TSH-INDUCED STIMULATION OF THYROIDAL PROTEIN SYNTHESIS IN THE RAT

1974 ◽  
Vol 77 (1) ◽  
pp. 64-70 ◽  
Author(s):  
Gustav Wägar
Keyword(s):  
Protein Synthesis ◽  
Actinomycin D ◽  
The Other ◽  
Leucine Incorporation ◽  
Short Term ◽  
Other Hand ◽  
Thyroid Glands ◽  
Translational Level ◽  
Stimulation Of

ABSTRACT Whether the short-term regulation of thyroidal protein synthesis by TSH occurs at the transcriptional or the translational level was tested by measuring the effect of actinomycin D (act D) on the TSH-induced stimulation of L-14C-leucine incorporation into the thyroidal proteins of rats. TSH was injected 6 h before the rats were killed. The thyroid glands were then removed and incubated in vitro in the presence of L-14C-leucine for 2 h. The pronounced stimulation of leucine incorporation in the TSH-treated animals was depressed as compared with controls but still significant even when the animals had been pre-treated with 100 μg act D 24 and 7 h before sacrifice. On the other hand, act D strongly decreased incorporation of 3H-uridine into RNA. Short-term regulation of thyroidal protein synthesis by TSH appears to be partly but not wholly dependent on neosynthesis of RNA. Hence regulation may partly occur at the translation level of protein synthesis.

Electrical stimulation of the carotid sinus lowers arterial pressure and improves heart rate variability in l-NAME hypertensive conscious rats

2020 ◽  
Vol 43 (10) ◽  
pp. 1057-1067 ◽  
Author(s):  
Gean Domingos-Souza ◽  
Fernanda Machado Santos-Almeida ◽  
César Arruda Meschiari ◽  
Nathanne S. Ferreira ◽  
Camila A. Pereira ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Conscious Rats ◽  
Stimulation Of

scholarly journals Receptor-operated Ca2+ channels in gastric parietal cells: gastrin and carbachol induce Ca2+ influx in depleting intracellular Ca2+ stores

1993 ◽  
Vol 289 (1) ◽  
pp. 117-124 ◽  
Author(s):  
S Roche ◽  
J P Bali ◽  
R Magous
Keyword(s):  
Steady State ◽  
Receptor Activation ◽  
Parietal Cells ◽  
The Other ◽  
Bivalent Cation ◽  
Gtp Binding ◽  
Gastric Parietal Cells ◽  
Type Receptor ◽  
Ca2 Channels ◽  
Stimulation Of

The mechanism whereby gastrin-type receptor and muscarinic M3-type receptor regulate free intracellular Ca2+ concentration ([Ca2+]i) was studied in rabbit gastric parietal cells stimulated by either gastrin or carbachol. Both agonists induced a biphasic [Ca2+]i response: a transient [Ca2+]i rise, followed by a sustained steady state depending on extracellular Ca2+. Gastrin and carbachol also caused a rapid and transient increase in Mn2+ influx (a tracer for bivalent-cation entry). Pre-stimulation of cells with one agonist drastically decreased both [Ca2+]i increase and Mn2+ influx induced by the other. Neither diltiazem nor pertussistoxin treatment had any effect on agonist-stimulated Mn2+ entry. Thapsigargin, a Ca(2+)-pump inhibitor, induced a biphasic [Ca2+]i increase, and enhanced the rate of Mn2+ entry. Preincubation of cells with thapsigargin inhibits the [Ca2+]i increase as well as Mn2+ entry stimulated by gastrin or by carbachol. Thapsigargin induced a weak but significant increase in Ins(1,4,5)P3 content, but this agent had no effect on the agonist-evoked Ins(1,4,5)P3 response. In permeabilized parietal cells, Ins(1,4,5)P3 and caffeine caused an immediate Ca2+ release from intracellular pools, followed by a reloading of Ca2+ pools which can be prevented in the presence of thapsigargin. We conclude that (i) gastrin and carbachol mobilize common Ca2+ intracellular stores, (ii) Ca2+ permeability secondary to receptor activation involves neither a voltage-sensitive Ca2+ channel nor a GTP-binding protein from the G1 family, and (iii) agonists regulate common Ca2+ channels in depleting intracellular Ca2+ stores.

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