Plasma Glycerol Concentrations Research Articles

Mechanism of changes induced in plasma glycerol by scent stimulation with grapefruit and lavender essential oils

In a previous study, we found that stimulation with scent of grapefruit oil (SGFO) elevated plasma glycerol levels in rats. However, stimulation with scent of lavender oil (SLVO) triggered a negative effect. To identify the mechanism of these changes during lipolysis, we examined the role of autonomic blockers and bilateral lesions of the hypothalamic suprachiasmatic nucleus (SCN) in the modification of plasma glycerol in rats exposed to SGFO and SLVO. We found that intraperitoneal injection of propranolol hydrochloride and atropine sulfate eliminated the changes in plasma glycerol levels induced by SGFO and SLVO, respectively. Bilateral lesions of the SCN completely abolished the effects of SGFO and SLVO on lipolysis. In addition, we investigated tyrosine phosphorylation of the transmembrane glycoprotein BIT (a brain immunoglobulin-like molecule with tyrosine-based activation motifs, a member of the signal-regulator protein family), which was found to be involved in the activation of renal sympathetic nerves and increase in body temperature on cold exposure. SGFO was found to enhance the immunoreactivity of BIT to the 4G10 anti-phosphotyrosine antibody in the SCN, whereas SLVO decreased the immunoreactivity. The changes in BIT phosphorylation resulting from the exposure to SGFO and SLVO were eliminated by the corresponding histamine receptor antagonists, which eliminated the changes in plasma glycerol concentration. The results suggest that SGFO and SLVO affect the autonomic neurotransmission and lipolysis. The SCN and histamine neurons are involved in the lipolytic responses to SGFO and SLVO, and tyrosine phosphorylation of BIT is implicated in the relevant signaling pathways.

Effects of Resistance Exercise on Lipolysis during Subsequent Submaximal Exercise

This study examined effects of prior resistance exercise on fat metabolism during subsequent submaximal exercise with different recovery periods between exercise bouts. Ten male subjects performed three types of exercise regimens: 1) submaximal endurance exercise only (E), 2) submaximal endurance exercise with prior resistance exercise and 20 min of rest (RE20), and 3) submaximal endurance exercise with prior resistance exercise and 120 min of rest (RE120). Resistance exercise consisted of six exercises, each with three to four sets at 10-repetition maximum. Subjects performed cycle ergometer exercise at 50% of the maximal oxygen uptake for 60 min. Prior resistance exercise caused increases in blood lactate, plasma norepinephrine, serum growth hormone (GH), insulin, and glycerol concentrations (P < 0.01). Before the submaximal exercise, serum free fatty acid (FFA) concentration was higher in the RE120 than in the RE20 and E trials (P < 0.01), although concentrations of plasma norepinephrine, serum GH, insulin, and glycerol were higher in the RE20 than in the RE120 and E trials (P < 0.05). Concentrations of FFA and glycerol during the 60-min submaximal exercise were higher in the RE120 and RE20 trials than in the E trial (P < 0.05). No significant difference was observed in the acetoacetate and 3-hydroxybutyrate responses. In the RE20 trial, fat oxidation throughout the 60-min submaximal exercise (mean value) was greater than in the E trial (P < 0.05), but no significant difference was found between the RE120 and E trials. Fat availability during the submaximal exercise was enhanced by prior resistance exercise. However, augmentation of fat oxidation was observed only in the trial with shorter rest between resistance exercise and submaximal exercise bouts (RE20 trial).

Deletion of the gene encoding the islet-specific glucose-6-phosphatase catalytic subunit-related protein autoantigen results in a mild metabolic phenotype

Islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP, now known as glucose-6-phosphatase, catalytic, 2 [G6PC2]) has recently been identified as a major autoantigen in mouse and human type 1 diabetes. Strategies designed to suppress expression of the gene encoding G6PC2 might therefore be useful in delaying or preventing the onset of this disease. However, since the function of G6PC2 is unclear, the concern with such an approach is that a change in G6PC2 expression might itself have deleterious consequences. To address this concern and assess the physiological function of G6PC2, we generated G6pc2-null mice and performed a phenotypic analysis focusing principally on energy metabolism. No differences in body weight were observed and no gross anatomical or behavioural changes were evident. In 16-week-old animals, following a 6-h fast, a small but significant decrease in blood glucose was observed in both male (-14%) and female (-11%) G6pc2 (-/-) mice, while female G6pc2 (-/-) mice also exhibited a 12% decrease in plasma triacylglycerol. Plasma cholesterol, glycerol, insulin and glucagon concentrations were unchanged. These results argue against the possibility of G6PC2 playing a major role in pancreatic islet stimulus secretion coupling or energy homeostasis under physiological conditions imposed by conventional animal housing. This indicates that manipulating the expression of G6PC2 for therapeutic ends may be feasible.

Exploring the Potential Ergogenic Effects of Glycerol Hyperhydration

During athletic competition or recreational pursuits, a body's hydration level can become compromised, resulting in a decrement in performance. Glycerol (1,2,3-propanetriol) has been used to induce hyperhydration in an attempt to offset the deleterious effects of dehydration. When glycerol is consumed orally, it is rapidly absorbed primarily in the small intestine. It is reported to be evenly distributed among all fluid compartments, with the exception of the cerebral spinal fluid and aqueous humour, and promotes hyperhydration by inducing an osmotic gradient. Through an increase in the kidney's medullary concentration gradient, water absorption in the nephron is enhanced. When glycerol is consumed, the plasma glycerol concentration increases in proportion to the dose ingested, which easily exceeds the glycerol saturation point resulting in urinary glycerol excretion. Thus, without supplemental glycerol ingestion, there will be a decrease in the osmotic gradient resulting in a loss of hyperhydration. The ergogenic nature of glycerol has been investigated as to its effect on fluid retention, thermoregulation, cardiovascular responses and performance. While many studies provide evidence of hyperhydration, others do not. Only two studies reviewed showed a thermoregulatory advantage. Furthermore, the preponderance of evidence neither weighed for or against cardiovascular or performance advantages. What makes one study provide favourable results while another study does not is unclear. Possible explanations may include subject characteristics, environmental factors, research design, whether fluids with or without glycerol were given during exercise, the rate at which fluids are initially given to induce hyperhydration, the time between peak hyperhydration/peak plasma glycerol concentration and the trial (i.e. exercise), the glycerol dose (i.e. 1.0 g/kg body mass) and what it is based upon, the percentage glycerol solution (i.e. 5%, 20%), the variation of time between the end of the hydration protocol and the beginning of exercise, or perhaps the intensity of exercise (fixed, variable, percentage maximum oxygen uptake). What is clear is that glycerol has the capacity to enhance fluid retention. In so doing, glycerol hyperhydration may be a logistically preferred method due to concomitant decrease in urine output and free-water clearance, which may give a performance advantage by offsetting dehydration. Future research should focus on maintaining plasma glycerol concentrations at levels necessary to maintain osmotic forces required to support continued hyperhydration. Potential benefits of glycerol should be further explored to identify the circumstances or factors that may contribute to an ergogenic effect.

Green tea extract ingestion increases fat oxidation during exercise in humans

PURPOSE: To study the effect of acute ingestion of green tea extract on fat oxidation during exercise in humans. METHODS: In a cross over study design 11 healthy males (26 ± 2 y) performed two exercise trials separated by at least one week. All participants kept a 24-hour food diary prior to the first trial, which was replicated prior to the second trial. During this 24 hour period, participants ingested three capsules containing either green tea extract (928 ± 15 mg total polyphenols of which 390 ± 6 mg was EGCG)(GTE) or a corn-flour placebo (1298 ± 25 mg) (PLA). Each trial consisted of 30-min cycling at 50% of maximal power output (Wmax). Rates of whole body substrate metabolism were determined via indirect calorimetry. RESULTS: There were no differences in oxygen uptake between the GTE or PLA trials. Energy expenditure was elevated by 3% following GTE ingestion (10.9 ± 0.54 vs 11.3 ± 0.52 kcal·min−1, PLA & GTE respectively, p<0.05). Average fat oxidation rates for the 30-min exercise trial were elevated by 17.5% following GTE ingestion when compared to PLA (0.34 ± 0.03 vs 0.40 ± 0.03 g·min−1, PLA & GTE respectively, p<0.05). Plasma FFA concentrations were similar between trials, however, plasma glycerol concentrations were elevated following GTE ingestion (123 ± 12 vs 102 ± 6 μmol·L−1, GTE & PLA respectively, p<0.05). CONCLUSION: Green tea extract ingestion can increase fat oxidation during exercise in humans.

Chronological Approach of Diet‐induced Alterations in Muscle Mitochondrial Functions in Rats

Mitochondrial dysfunction might predispose individuals to develop insulin resistance. Our objective was to determine whether mitochondrial dysfunction or insulin resistance was the primary event during high-fat (HF) diet. Rats were fed an HF diet for 0, 3, 6, 9, 14, 20, or 40 days and compared with control. Soleus and tibialis muscle mitochondrial activity were assessed using permeabilized fiber technique. Insulin [area under the curve for insulin (AUC(I))] and glucose [area under the curve for glucose (AUC(G))] responses to intraperitoneal glucose tolerance test as well as fasting plasma non-esterified fatty acids (NEFAs), triglyceride, and glycerol concentrations were determined. AUC(I) and AUC(G) were altered from Day 6 (p < 0.01 vs. Day 0). In soleus, oxidative phosphorylation (OXPHOS) activity was transiently enhanced by 26% after 14 days of HF diet (p < 0.05 vs. Day 0) conjointly with 62% increase in NEFA concentration (p < 0.05 vs. Day 0). This was associated with normalized AUC(G) at Day 14 and with a decline of plasma NEFA concentration together with stabilization of intra-abdominal adiposity at Day 20. Prolongation of HF diet again caused an increase in plasma NEFA concentration, intra-abdominal adiposity, AUC(I), and AUC(G). At Day 40, significant decrease in OXPHOS activity was observed in soleus. Mitochondria first adapt to overfeeding in oxidative muscle limiting excess fat deposition. This potentially contributes to maintain glucose homeostasis. Persistent overfeeding causes insulin resistance and results in a slow decline in oxidative muscle OXPHOS activity. This shows that the involvement of mitochondria in the predisposition to insulin resistance is mainly due to an inability to face prolonged excess fat delivery.

Autonomic and cardiovascular responses to scent stimulation are altered in cry KO mice

Previously, we observed that in rats, olfactory stimulation with scent of grapefruit oil (SGFO) elevates the activities of sympathetic nerves. SGFO also suppresses gastric vagal (parasympathetic) nerve activity (GVNA), increases the plasma glycerol concentration, blood pressure (BP) and body temperature, and reduces appetite. In contrast, olfactory stimulation with scent of lavender oil (SLVO) has opposite effects in rats. Here, we show that in mice, olfactory stimulation with SGFO elevated activities of sympathetic nerves innervating the kidney, adrenal gland and brown adipose tissue as well as increasing BP and suppressing GVNA, whereas olfactory stimulation with SLVO decreased these sympathetic nerve activities and BP, and elevated GVNA. Electrolytic lesions of the mouse hypothalamic suprachiasmatic nucleus (SCN) eliminated changes in renal sympathetic nerve activity (RSNA), BP and GVNA induced by either SGFO or SLVO. Furthermore, SGFO-induced elevations in RSNA and BP and the SLVO-induced GVNA increase were not observed in Cryptochrome (Cry)-deficient mice, which harbor mutations in both cry1 and cry2 and lack normal circadian rhythms. These findings suggest that SGFO and SLVO affect autonomic neurotransmission and BP via the SCN in mice. Moreover, the molecular clock mechanism in the SCN, which involves the cry1 and cry2 genes, is partially involved in mediating these autonomic and cardiovascular actions of SGFO and SLVO.

Acute hyperinsulinemia inhibits intramyocellular triglyceride synthesis in high-fat-fed obese rats

Hyperinsulinemia is common in obesity, but whether it plays a role in intramyocellular triglyceride (imcTG) buildup is unknown. In this study, hyperinsulinemic-euglycemic clamp experiments were performed in overnight-fasted lean and high-fat-fed obese rats, awake, to determine the effect of insulin on imcTG synthesis (incorporation of [(14)C]glycerol, [(14)C]glucose, and [(3)H]oleate). Insulin infusion at 25 (low insulin) and 100 (high insulin) pmol/kg/min increased plasma insulin by 5- and 16-fold, respectively, whereas plasma and intramyocellular glycerol, FFAs, triglycerides, and glucose levels were maintained at their basal levels by co-infusion of exogenous glycerol, FFAs, and triglycerides at fixed rates and glucose at varying rates. In obese rats, insulin suppressed incorporation of glycerol into the imcTG-glycerol moiety dose dependently (P < 0.01-P < 0.001) in gastrocnemius and tibialis anterior, but only the high insulin suppressed it in soleus (P < 0.05). The low insulin suppressed glucose incorporation into imcTG-glycerol in all three muscles (P = 0.01-P < 0.01). However, the low insulin did not affect (P > 0.05) and the high insulin suppressed (P < 0.05-P < 0.01) fatty acid incorporation into imcTG in all three muscles. Insulin also suppressed glycerol incorporation in lean rats (P < 0.01-P < 0.04). On the other hand, imcTG pool size was not affected by insulin (P > 0.05). These observations suggest that acute hyperinsulinemia inhibits imcTG synthesis and thus does not appear to promote imcTG accumulation via the synthetic pathway, at least in the short term.

Effect of different intensities of active recovery on sprint swimming performance

Active recovery reduces blood lactate concentration faster than passive recovery and, when the proper intensity is applied, a positive effect on performance is expected. The purpose of the study was to investigate the effect of different intensities of active recovery on performance during repeated sprint swimming. Nine male well-trained swimmers performed 8 repetitions of 25 m sprints (8 x 25 m) interspersed with 45 s intervals, followed by a 50 m sprint test 6 min later. During the 45 s and 6 min interval periods, swimmers either rested passively (PAS) or swam at an intensity corresponding to 50% (ACT50) and 60% (ACT60) of their individual 100 m velocity. Blood lactate was higher during PAS compared with ACT50 and ACT60 trials (p < 0.05), whereas plasma ammonia and glycerol concentration were not different between trials (p > 0.05). Mean performance time for the 8 x 25 m sprints was better in the PAS compared with the ACT50 and ACT60 trials (PAS: 13.10 +/- 0.07 vs. ACT50: 13.43 +/- 0.10 and ACT60: 13.47 +/- 0.10s, p < 0.05). The first 25 m sprint was not different across trials (p > 0.05), but performance decreased after sprint 2 during active recovery trials (ACT50 and ACT60) compared with the passive recovery (PAS) trial (p < 0.05). Performance time for the 50 m sprint performed 6 min after the 8 x 25 m sprints was no different between trials (p > 0.05). These results indicate that active recovery at intensities corresponding to 50% and 60% of the 100 m velocity during repeated swimming sprints decreases performance. Active recovery reduces blood lactate concentration, but does not affect performance on a 50 m sprint when 6 min recovery is provided. Passive recovery is advised during short-interval repeated sprint training in well-trained swimmers.

Effects of dietary glycaemic response after exercise on blood concentrations of substrates used indirectly for muscle glycogenesis

Exercise depletes muscle glycogen stores, which could subsequently impair performance. Muscle glycogen replenishment is determined by substrate availability. To study the effects of feeding meals of varying glycaemic responses on blood concentrations of substrates used for glycogenesis in horses with exercise-induced glycogen depletion. In a 3-way crossover study, 7 horses received each of 3 isocaloric diets for 72 h after undergoing glycogen-depleting exercise: 1) a high soluble-carbohydrate diet, which induced a high-glycaemic (HGI) response; 2 and 3) a low soluble-carbohydrate or a mixed soluble-carbohydrate diet (control group), which both induced a similar low-to-moderate glycaemic (LGI) response. Muscle biopsies and venous samples were collected before and up to 72 h after exercise. Feeding HGI diet resulted in a higher (P<0.001) rate of muscle glycogenesis over 72 h compared to LGI diets. Plasma glycerol, triglyceride, lactate, serum NEFA and total protein concentrations, and haematocrit were significantly (P<0.001) higher after compared to before exercise. Whereas no significant overall dietary effect was observed on these metabolites over 72 h, there was a tendency for glycerol, NEFA and triglyceride concentrations to be lower for LGI compared to HGI diets over 6 h after exercise (P<0.05; 1, 6 and 4-6 h after exercise, respectively). These data suggest that horses fed LGI meals after exercise had limited lipid utilisation without any significant shift of substrate utilisation toward gluconeogenesis, which could have contributed to the slower rate of muscle glycogenesis compared to horses fed HGI diets.

Influence of high-carbohydrate mixed meals with different glycemic indexes on substrate utilization during subsequent exercise in women1,2

Few data exist on the metabolic responses to mixed meals with different glycemic indexes and their effects on substrate metabolism during exercise in women. We examined the effects of preexercise mixed meals providing carbohydrates with high (HGI) or low glycemic index (LGI) on substrate utilization during rest and exercise in women. Eight healthy, active, eumenorrheic women [aged 18.6 +/- 0.9 y; body mass: 59.9 +/- 7.1 kg; maximal oxygen uptake (VO(2)max): 48.7 +/- 1.1 mL . kg(-1) . min(-1)] completed 2 trials. On each occasion, subjects were provided with a test breakfast 3 h before performing a 60-min run at 65% VO(2)max on a motorized treadmill. Both breakfasts provided 2 g carbohydrate/kg body mass and were isoenergetic. The calculated GIs of the meals were 78 (HGI) and 44 (LGI). Peak plasma glucose and serum insulin concentrations were greater after the HGI breakfast than after the LGI breakfast (P < 0.05). No significant differences in substrate oxidation were reported throughout the postprandial period. During exercise, the estimated rate of fat oxidation was greater in the LGI trial than in the HGI trial (P < 0.05). Similarly, plasma free fatty acid and glycerol concentrations were higher throughout exercise in the LGI trial (P < 0.05). No significant differences in plasma glucose or serum insulin were observed during exercise. Altering the GI of the carbohydrate within a meal significantly changes the postprandial hyperglycemic and hyperinsulinemic responses in women. A LGI preexercise meal resulted in a higher rate of fat oxidation during exercise than did an HGI meal.

Influence of high-carbohydrate mixed meals with different glycemic indexes on substrate utilization during subsequent exercise in women1,2

Background: Few data exist on the metabolic responses to mixed meals with different glycemic indexes and their effects on substrate metabolism during exercise in women. Objective: We examined the effects of preexercise mixed meals providing carbohydrates with high (HGI) or low glycemic index (LGI) on substrate utilization during rest and exercise in women. Design: Eight healthy, active, eumenorrheic women [aged 18.6 ± 0.9 y; body mass: 59.9 ± 7.1 kg; maximal oxygen uptake (V̇O2max): 48.7 ± 1.1 mL · kg−1 · min−1] completed 2 trials. On each occasion, subjects were provided with a test breakfast 3 h before performing a 60-min run at 65% V̇O2max on a motorized treadmill. Both breakfasts provided 2 g carbohydrate/kg body mass and were isoenergetic. The calculated GIs of the meals were 78 (HGI) and 44 (LGI). Results: Peak plasma glucose and serum insulin concentrations were greater after the HGI breakfast than after the LGI breakfast (P < 0.05). No significant differences in substrate oxidation were reported throughout the postprandial period. During exercise, the estimated rate of fat oxidation was greater in the LGI trial than in the HGI trial (P < 0.05). Similarly, plasma free fatty acid and glycerol concentrations were higher throughout exercise in the LGI trial (P < 0.05). No significant differences in plasma glucose or serum insulin were observed during exercise. Conclusion: Altering the GI of the carbohydrate within a meal significantly changes the postprandial hyperglycemic and hyperinsulinemic responses in women. A LGI preexercise meal resulted in a higher rate of fat oxidation during exercise than did an HGI meal.

Exercise Induced Energy Deficit Does Not Impact Resting Plasma Free Fatty Acids and Glycerol

Recently, negative energy balance induced by decreased energy intake was reported to cause resting plasma free fatty acid and glycerol concentrations to increase (1). Whether negative energy balance induced by increased energy expenditure affects biomarkers of lipid metabolism similarly is not known. PURPOSE: To compare effects of energy deficit induced by increased daily exercise on plasma markers of lipolyis with effects of increased exercise without energy deficit. METHODS: Fourteen men (23.4 ± 1.3 yrs, 74.0 ± 1.8 kg, 14.4 ± 1.4 % body fat, VO2peak58.2 ± 2.2 ml/kg/min) consumed a diet containing ∼55% CHO, 38% fat, and 0.9g protein/kg/d for 11 days. Day 1–4 (baseline, BL) energy intake (EI) matched EI and energy expenditure (EE) recorded the week before BL. Volunteers then added exercise at 55–65% VO2peak to expend an additional 1000 kcal/d for 7 days (EX). Seven volunteers increased EI to maintain energy balance (BAL), while seven maintained BL EI (DEF). EE was assessed by closed circuit spirometry, and body weight was recorded daily. Fasting plasma was analyzed for free fatty acid (FFA) and glycerol on days 3, 6, and 11. RESULTS: EI and EE for BAL was 3642 ± 271 and 3659 ± 276 kcal/d during BL and increased to 4594 ± 266 and 4655 ± 274 kcal/d during EX. EI for DEF was 3450 ± 97 kcal/d for BL and EX, while EE increased from 3491 ± 151 to 4447 ± 157 kcal/d for BL and EX respectively. BAL remained weight stable, while DEF lost 2.4 ± 0.21 kg (p<0.05). Resting FFA and glycerol values (mean ± SEM) are shown. * Difference between groups (p<0.05)TableThere were no differences within either group for FFA or glycerol from BL to EX. CONCLUSION: In contrast to what was observed with a one-day diet-induced energy deficit, a 7-d 1000 kcal/d exercise-induced energy deficit did not affect plasma markers of lipolysis, suggesting differential lipolytic regulation during dietary and exercise-induced energy deficit.

Acute Experimental Mastitis Is Not Causal Toward the Development of Energy-Related Metabolic Disorders in Early Postpartum Dairy Cows

Twenty Holstein cows in early lactation (7 d in milk) were administered 100μg of Escherichia coli lipopolysaccharide (LPS) dissolved in 10mL of sterile 0.9% NaCl saline (treatment; TRT) or 10mL of sterile saline (control) into both right mammary quarters to test the hypothesis that acute experimental mastitis would have negative impacts on aspects of energy metabolism that might lead to the development of metabolic disorders. A primed continuous intravenous infusion (14-μmol/kg of BW priming dose; 11.5-μmol/kg of BW per h continuous infusion) of 6,6-dideuterated glucose was used to determine pre- and posttreatment glucose kinetics using steady-state tracer methodologies. The LPS-treated cows displayed productive, clinical, and physiological signs of moderate to severe inflammation; control cows displayed no signs of immune activation. Pretreatment glucose rates of appearance (Ra) into plasma were similar (715 and 662±33 mmol/h for TRT and control, respectively) between treatment groups. Intramammary LPS infusion into TRT cows resulted in increased glucose Ra relative to control cows (mean glucose Ra from 150 through 270min after intramammary infusion were 815 and 674±21 mmol/h for TRT and control cows, respectively). Furthermore, plasma concentrations of glucose increased, whereas plasma nonesterified fatty acids, glycerol, and β-hydroxybutyrate concentrations decreased, in TRT relative to control cows. Interestingly, plasma insulin concentration increased dramatically in TRT cows and occurred prior to the small increase in plasma glucose concentration. Although these results only represent the early stages of inflammation, they are not consistent with a causal relationship between mastitis and energy-related metabolic disorders and instead suggest a coordinated protective effect by the immune system on metabolism during the early stages of mammary insult.

Olfactory stimulation with scent of lavender oil affects autonomic neurotransmission and blood pressure in rats

Previously, we observed that olfactory stimulation with scent of lavender oil (SLVO) suppressed sympathetic nerve activities and elevated gastric vagal (parasympathetic) nerve activity (GVNA), decreased plasma glycerol concentration and body temperature, and enhanced appetite in rats. Here, we further showed that olfactory stimulation with SLVO lowered renal sympathetic nerve activity (RSNA) and blood pressure (BP) and elevated GVNA in urethane-anesthetized rats. Olfactory stimulation with linalool, a component of lavender oil, also elicited decreases in RSNA and BP and an increase in GVNA in urethane-anesthetized rats. Anosmia induced by pretreatment of the nasal cavity by application of ZnSO 4 eliminated the effects of both SLVO and scent of linalool on RSNA, GVNA and BP. Furthermore, intracerebroventricular administration of thioperamide, a histaminergic H3-antagonist, abolished the suppression of RSNA and BP as well as the elevation of GVNA mediated by both SLVO and scent of linalool. Finally, bilateral lesions of the hypothalamic suprachiasmatic nucleus (SCN) eliminated RSNA and BP suppression and the elevation of GVNA due to SLVO or linalool. Thus, it was concluded that scent of lavender oil and its active component, linalool, affects autonomic neurotransmission and reduces blood pressure through the central histaminergic nervous system and the SCN.

Metabolic fate of a large amount of 13C-glycerol ingested during prolonged exercise

We have shown that the oxidation rate of exogenous glycerol and glucose during prolonged exercise were similar when ingested in small amounts (0.36 g/kg) (J Appl Physiol 90:1685,2001). The oxidation rate of exogenous carbohydrate increases with the amount ingested. We, thus, hypothesized that the oxidation rate of exogenous glycerol would also be larger when ingested in large amount. The study was conducted on six male subjects exercising for 120 min at 64 (2)% VO(2)max while ingesting 1 g/kg of (13)C-glycerol. Substrate oxidation was measured using indirect respiratory calorimetry corrected for protein oxidation, and from V(13)CO(2) at the mouth. The (13)C enrichment of plasma glucose was also measured in order to follow the possible conversion of (13)C-glycerol into glucose. In spite of the large amount of glycerol ingested and absorbed (plasma glycerol concentration = 8.0 (0.3) mmol/l at min 100), exogenous glycerol oxidation over the last 80 min of exercise [8.8 (1.6) g providing 4.1 (0.7)% of the energy yield] was similar to that observed when 0.36 g/kg was ingested. The comparison between the (13)C enrichment of plasma glucose and the oxidation rate of (13)C-glycerol showed that a portion of exogenous glycerol was converted into glucose before being oxidized, but also suggested that another portion could have been directly oxidized in peripheral tissues.

Olfactory stimulation with scent of essential oil of grapefruit affects autonomic neurotransmission and blood pressure

Previously, we observed that olfactory stimulation with scent of grapefruit oil (SGFO) enhances sympathetic nerve activities and suppresses gastric vagal (parasympathetic) nerve activity (GVNA), increases plasma glycerol concentration and body temperature, and decreases appetite in rats. Here, we show that olfactory stimulation with SGFO for 10 min elevates renal sympathetic nerve activity (RSNA) and blood pressure (BP) and lowers GVNA in urethane-anesthetized rats. Olfactory stimulation with limonene, a major component of grapefruit oil, also elicited increases in RSNA and BP in urethane-anesthetized rats. Anosmic treatment with ZnSO 4 eliminated both the effects of SGFO and scent of limonene on RSNA and BP. Intracerebral administration of diphenhydramine, a histaminergic H1-antagonist, abolished SGFO- or scent of limonene-mediated increases in RSNA and BP as well as the decrease in GVNA. Moreover, bilateral lesions of the hypothalamic suprachiasmatic nucleus (SCN) eliminated the SGFO- and limonene-mediated increases in RSNA and BP and decrease in GVNA, but bilateral lesions of the cerebral cortex did not have any affect on these parameters. These findings suggest that scent of grapefruit oil and its active component, limonene, affect autonomic neurotransmission and blood pressure through central histaminergic nerves and the suprachiasmatic nucleus.

Physiological adaptations to fasting in an actively wintering canid, the Arctic blue fox (Alopex lagopus)

This study investigated the physiological adaptations to fasting using the farmed blue fox (Alopex lagopus) as a model for the endangered wild arctic fox. Sixteen blue foxes were fed throughout the winter and 32 blue foxes were fasted for 22 d in Nov-Dec 2002. Half of the fasted blue foxes were food-deprived again for 22 d in Jan-Feb 2003. The farmed blue fox lost weight at a slower rate (0.97-1.02% body mass d(-1)) than observed previously in the arctic fox, possibly due to its higher initial body fat content. The animals experienced occasional fasting-induced hypoglycaemia, but their locomotor activity was not affected. The plasma triacylglycerol and glycerol concentrations were elevated during phase II of fasting indicating stimulated lipolysis, probably induced by the high growth hormone concentrations. The total cholesterol, HDL- and LDL-cholesterol, urea, uric acid and total protein levels and the urea:creatinine ratio decreased during fasting. Although the plasma levels of some essential amino acids increased, the blue foxes did not enter phase III of starvation characterized by stimulated proteolysis during either of the 22-d fasting procedures. Instead of excessive protein catabolism, it is liver dysfunction, indicated by the increased plasma bilirubin levels and alkaline phosphatase, alanine aminotransferase and aspartate aminotransferase activities, that may limit the duration of fasting in the species.

Energy deficit without reducing dietary carbohydrate alters resting carbohydrate oxidation and fatty acid availability

Reduced carbohydrate (CHO) availability after exercise has a potent influence on the regulation of substrate metabolism, but little is known about the impact of fat availability and/or energy deficit on fuel metabolism when dietary CHO availability is not reduced. The purpose of this study was to determine the influence of a postexercise energy deficit, independent of CHO availability, on plasma substrate concentrations and substrate oxidation. Seven moderately trained men (peak oxygen uptake: 56 +/- 2 ml.kg(-1).min(-1)) performed exhaustive cycling exercise on two separate occasions. The two trials differed only by the meals ingested after exercise: 1) a high-fat diet designed to maintain energy balance or 2) a low-fat diet designed to elicit energy deficit. The CHO and protein contents of the diets were identical. The next morning, we measured plasma substrate and insulin concentrations and CHO oxidation, and we obtained muscle biopsies from the vastus lateralis for measurement of pyruvate dehydrogenase kinase (PDK)-2 and PDK-4 mRNA expression by using RT-PCR. Despite identical blood glucose (5.0 +/- 0.1 and 4.9 +/- 0.1 mM) and insulin (7.9 +/- 1.1 and 8.4 +/- 0.9 microU/ml) concentrations, plasma fatty acid and glycerol concentrations were elevated three- to fourfold during energy deficit compared with energy balance and CHO oxidation was 40% lower (P < 0.01) the morning after energy deficit compared with energy balance (328 +/- 69 and 565 +/- 89 micromol/min). The lower CHO oxidation was accompanied by a 7.3 +/- 2.5-fold increase in PDK-4 mRNA expression after energy deficit (P < 0.05), whereas PDK-2 mRNA was similar between the trials. In conclusion, energy deficit increases fatty acid availability, increases PDK-4 mRNA expression, and suppresses CHO oxidation even when dietary CHO content is not reduced.

Response to Intra- and Extracellular Lipolytic Agents and Hormone-Sensitive Lipase Translocation Are Impaired in Adipocytes from Rats Adapted to a High-Protein, Carbohydrate-Free Diet

We showed previously that rats adapted to a high-protein (70%), carbohydrate-free (HP) diet have reduced lipolytic activity. To clarify the underlying biochemical mechanisms, several metabolic processes involved in adipose tissue lipolysis were investigated. The experiments were performed in rats adapted for 15 d to an HP or a balanced diet. In agreement with previous results, microdialysis experiments showed that the concentrations of adipose tissue interstitial and arterial plasma glycerol were lower in rats adapted to the HP diet. Under nonstimulated conditions, rates of lipolysis, estimated by glycerol release to the incubation medium, were reduced in adipocytes from HP rats. Under the same conditions, there was a small, but significant (17%) reduction in the activity of hormone sensitive lipase (HSL), with no change in the content of the enzyme. Upon stimulation with isoproterenol, the percentage of the enzyme in the adipocyte cytosol translocated to the fat droplet was 20-25%in HP rats and 40-50% in rats fed the balanced diet. Adipocytes from HP diet-adapted rats had a significantly reduced response (approximately 40%) to the lipolytic action of nonspecific (norepinephrine, epinephrine, isoproterenol) and specific (CL316,243, BRL37,344, dobutamine, clenbuterol) beta-adrenergic agonists. Adipocytes from HP rats also had a reduced lipolytic response to the intracellular agents, dibutyryl cAMP (44%), forskolin (46%), and isobutyl-methylxanthine (29%). The data suggest that the main mechanism responsible for the reduced basal and stimulated lipolysis in HP diet-adapted rats is an impairment in the intracellular process of lipolysis activation, with a deficient translocation of HSL to the fat droplet.