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Effects of cold acclimation and central opioid processes on thermoregulation in rats.

Two experiments, using centrally administered [D-Ala2-MePhe4-Gly(ol)5]enkephalin (DAMGO), a selective mu-opioid agonist, assessed the thermoregulatory consequences of cold acclimation. Experiment 1 assessed whether cold acclimation influenced DAMGO hyperthermia at room temperature. Sialo-adenectomized rats were implanted with ICV cannulae and IP Mini-Mitters. After 3 weeks of exposure to 5 degrees C (cold acclimation) or 22 degrees C (non-cold acclimation) rats were pretreated with IP naltrexone HCl (2 mg/kg b.wt.) or vehicle (0.15 M saline) and later administered a 5-microliters ICV injection of 0.15 M saline, 0.1, or 1.0 microgram DAMGO. Cold acclimation exerted little effect on core temperature but potentiated DAMGO hyperthermia in a dose-dependent, naltrexone-reversible, activity-independent manner. Experiment 2 assessed the effect these same manipulations exerted on operant escape from a convective source of mild heat (37 degrees C). Duration of heat escape increased with cold acclimation in a naltrexone-resistant manner, yet was not influenced by DAMGO in either non-cold-acclimated or cold-acclimated rats. These findings suggest that two central adaptations occur with cold acclimation: A non-mu-opioid process that increases heat sensitivity and a mu-opioid process that potentiates hyperthermia but fails to alter heat escape due to mu-opioid-mediated analgesia.

Acclimatization↗

A case study on the induction of clinical tolerance in cold urticaria.

The mechanism(s) by which repeated cold challenge in a patient with idiopathic acquired cold urticaria resulted in the induction of clinical tolerance to cold stimuli was studied. Plasma histamine levels, mast cell ultrastructure, and the cutaneous response to intradermal injections of morphine, histamine, and substance P were examined before and after the induction of tolerance. Plasma histamine levels draining cold-challenged, clinically tolerant skin were markedly diminished compared to histamine levels obtained during cold-induced angioedema. Furthermore, electronmicroscopy of skin samples taken from tolerant skin after cold challenge revealed intact, largely normal appearing mast cells. Intradermal injection of mast cell secretagogues and vasoactive agonists into normal and tolerant skin sites resulted in similar whealing responses. Thus, these studies suggest that the state of clinical tolerance to cold stimuli is due neither to mast cell-mediator depletion or tachyphylaxis of the cutaneous vasculature to vasoactive agonists. It appears likely that tolerance may be due to the induction of a specific state of unresponsiveness of mast cells to cold stimuli or possibly to depletion of a cold-induced cutaneous antigen capable of triggering mast cell degranulation.

Adaptation, Physiological↗

Effect of cold acclimation on the expression of glucose transporter Glut 4.

Glucose uptake by brown adipose tissue, measured following deoxyglucose injection in vivo, was increased by 6- and 11-fold following 2 and 14 days of cold exposure, respectively. To look for the possible mechanism of these modifications, the glucose transporter Glut 4 has been characterized at the protein and mRNA levels in brown adipose tissue, skeletal muscle and white adipose tissue following cold acclimation. Crude membranes were prepared from those tissues, and Glut 4 was studied by Western blot analysis. In brown adipose tissue, the total Glut 4 amount was increased by 52 +/- 7% and by 104 +/- 12% following 2 and 14 days of cold exposure, respectively. By contrast, in white adipose tissue of 14-day-cold-exposed mice the total Glut 4 content was decreased by 42 +/- 5%. However, Glut 4 concentration, expressed per mg of membrane protein, was unchanged in both brown and white adipose tissues following cold exposure, since the membrane protein content increased in brown but decreased in white adipose tissue. No modification in Glut 4 content was observed in skeletal muscle from cold-exposed mice. Total RNA were prepared and analyzed for Glut 4, glyceraldehyde phosphate dehydrogenase (GAPDH) and actin. Glut 4 and GAPDH mRNA were increased 2-fold in brown adipose tissue from cold-exposed mice, while actin mRNA content was unmodified. Glut 4 mRNA content was not changed in white adipose tissue and skeletal muscle from cold-exposed mice. Our results suggest that Glut 4 expression is differently modulated in the three insulin-responsive tissues during cold acclimation.

Acclimatization↗

Echinacea in the prevention of induced rhinovirus colds: a meta-analysis.

BACKGROUND: The therapeutic effectiveness of Echinacea in the treatment and the prevention of colds has been debated. Studies of naturally occurring colds are hampered by variability in time from onset of symptoms to treatment and by heterogeneity in trial design. Experimental infection studies allow for the standardization of time to initiation of treatment, virus type and dose, and immune competence of volunteers. OBJECTIVE: To determine whether the negative results obtained in previous studies of Echinacea were a consequence of efficacy or of inadequate sample size, we performed a meta-analysis of experimental rhinovirus infection studies on the efficacy of Echinacea extracts to prevent symptomatic development of an experimentally induced cold. METHODS: We carried out a systematic search of English- and German-language literature using the MEDLINE, EMBASE, CAplus, BIOSIS, CABA, AGRICOLA, TOXCENTER, SCISEARCH, NAHL, and NAPRALERT, databases and the search terms Echinacea, black Sampson, coneflower, and Roter Sonnenbut. Matching documents were then searched for > or = 1 of the following terms: rhinovirus, RV, inoculation, Inokulation, induced, induziert, artificial, and artifiziell. Suitable studies were identified and pooled for analysis. The primary end point was the development of symptomatic clinical colds, as defined by the authors of the original studies. Results were reported as differences in the proportion of subjects with symptomatic episodes of a common cold, expressed as odds ratios (ORs) and 95% CIs. The secondary outcome was the difference in total symptom severity scores between treatment groups (assessed daily by integrating the severity scores of 8 individual cold-related symptoms that were rated on a scale from 0 [absent] to 4 [very severe]). RESULTS: A total of 234 articles were identified through the literature search; 231 were excluded from the analysis because they related to studies of spontaneous common colds. Three suitable studies were selected for pooling of data. Based on the analysis, the likelihood of experiencing a clinical cold was 55% higher with placebo than with Echinacea (OR, 1.55 [95% CI, 1.02-2.36]; P<0.043). The absolute difference in total symptom scores between groups was -1.96 (95% CI, -4.83 to 0.90; P=NS). CONCLUSIONS: This meta-analysis suggests that standardized extracts of Echinacea were effective in the prevention of symptoms of the common cold after clinical inoculation, compared with placebo. Further prospective, appropriately powered clinical studies are required to confirm this finding.

Common Cold↗

Comparative cerebral responses to non-painful warm vs. cold stimuli in man: EEG power spectra and coherence.

AIMS: The cerebral processing of painful thermal (heat/cold) stimulation have been extensively studied, but little is known about cerebral activation to non-painful warm and cold stimuli. This study aimed to investigate the comparative EEG effects of warm vs. cold stimulus in man. MATERIALS AND METHODS: The left nondominant hands of 13 healthy male subjects were stimulated by non-painful warm (40-43 degrees C) and cold (12-15 degrees C) water. The somatic sensations were continuously assessed with an analogue visual scale device. EEG data (32 channels) recorded before, during and after the warm and cold stimulations were analysed quantitatively. RESULTS: No significant difference in intensity of sensation was found during warm and cold stimulations. Different patterns of EEG activity were superimposed on the similar background of EEG activation during and after warm and cold stimulations. Significant decrease of theta activity in contra-stimulus frontal region was observed during cold stimulation rather than warm stimulation. EEG power spectra in theta, alpha-1 and alpha-2 bands significantly increased after cold stimulation compared to baseline. EEG coherence in delta, alpha-1 and alpha-2 bands significantly increased in the contra-stimulus hemisphere during stimulations. CONCLUSION: This suggests that similar neural networks may process somatic warm and cold sensory inputs differently and the differential EEG patterns may be encoded by the qualities of thermal stimuli.

Adult↗

Chronic cold stress regulates ascending noradrenergic pathways.

Chronic exposure to cold in rats alters the activity of locus coeruleus (LC) neurons. In this study we aimed to examine the cellular effect of cold stress on catecholamine neurons, and determine whether this is specific to the LC compared with other catecholamine cell groups. Male Sprague-Dawley rats were subjected to 21 days of isolation under ambient conditions, chronic cold exposure at 5 degrees C, or after chronic cold followed by return to ambient temperature for 7 or 14 days. In the LC, chronic cold exposure significantly reduced tyrosine hydroxylase (TH) mRNA expression by approximately 45% compared with control rats, and remained significantly reduced (approximately 36%) after return to ambient conditions for 7 days; however, expression returned to normal after 14 days' recovery. There were no significant changes in TH mRNA in the substantia nigra or ventral tegmental area. Chronic cold increased expression of alpha2A adrenoceptor mRNA in the LC (approximately 27%). There were decreases in alpha2A expression in the nucleus tractus solitarius; however, this was seen only in rats returned to ambient conditions for 7 days. Additionally, alpha2A mRNA in the caudal ventrolateral medulla (A1 region) increased following cold exposure (approximately 84%) compared with controls. Binding of [125I]iodoclonidine to alpha2-like protein increased in the olfactory bulbs but decreased in the medial amygdala following cold exposure. Collectively, these data indicate robust effects of cold on central catecholamine neurons, not necessarily specific to the LC.

Afferent Pathways↗

Effects of cold- and heat hardening on thermal resistance in Drosophila melanogaster.

The effects of cold- and heat hardening on resistance to both low and high temperature stress was examined in Drosophila melanogaster lines selected for resistance to either cold or heat. The hardening effect was positive when the hardening was of the same type as the stress in all selection regimes. The effect of cold hardening on survival after heat stress was further examined in the lines selected for cold resistance and corresponding controls. A cross-protection effect (increased heat resistance after cold hardening) was present and this effect was lower in the lines selected for resistance to cold than in the controls. The level of Hsp70 expression induced by a non-lethal cold hardening was examined, showing that cold hardening induced Hsp70 expression. The results suggest that the cross-protection effect is at least partly due to Hsp70 expression induced by cold exposure.

Animals↗

Survival of Escherichia coli O157:H7 in frozen foods: impact of the cold shock response.

The survival of Escherichia coli O157:H7 strains in both frozen foods and trypticase soy broth (TSB) was investigated following cold shocking at 10 degrees C for 1.5 h. Using both trypticase soy agar (TSA) and violet red bile agar (VRBA) as recovery media, it was demonstrated that survival levels between cold shocked (CS) and non-cold shocked (NS) E. coli in ground beef or pork were not significantly different (P < or = 0.05). In contrast, cold shocking E. coli in either milk, whole egg or sausage resulted in a significant(P < or = 0.05) enhancement in survival. For milk, survival levels of CS E. coli, by 28 days of frozen storage, were 1.89 and 1.66 log10 cfu/ml higher on TSA and VRBA, respectively, when compared to NS cells. In egg these values were 0.64 and 1.31, while in sausage, values of 0.74 and 1.19 were obtained. In TSB (pH 7) survival of CS E. coli for some strains was about 3 log10 cfu/ml higher when compared to NS cells. Acidification of TSB (pH 5), however, appeared to negate the protective effects of the cold shock treatment. In milk, increasing the differential between the growth and cold shock temperatures resulted in higher numbers of survivors. In this regard the growth-cold shock temperature protocol giving optimum protection was 37-10 degrees C. In contrast, growth of E. coli at 20 degrees C followed by cold shocking at 10 degrees C did not result in any significant freeze protection. In addition, increased protection due to cold shocking was correlated with the appearance of a novel protein appearing at pI 4.8 following isoelectric focusing analysis, thus demonstrating an alteration of protein synthesis.

Animals↗

The effect of exercise training in cold on shivering and nonshivering thermogenesis in adult and aged C57BL/6J mice.

To understand the mechanisms of improvement of cold-induced heat production in aged mice following exercise training, the relative contributions of shivering and nonshivering thermogenesis to cold-induced metabolic responses were assessed in adult and aged C57BL/6J male mice, which inhabited sedentarily at room temperature, or were subjected either to a regimen of moderate intensity exercise training at 6 degrees C, or to sedentary repeated exposures to the same temperature. The main findings were that (1) aged mice had greater cold-induced nonshivering thermogenesis, but lower shivering than adult mice; (2) exercise training in a cold environment enhanced cold-induced nonshivering thermogenesis in adult mice, but suppressed it in aged animals; (3) exercise training in a cold environment increased shivering thermogenesis in both age groups, but this increase was much greater in aged mice; (4) the increase of cold-induced shivering thermogenesis was mainly responsible for increased cold tolerance in aged mice after exercise training in a cold environment.

Aging↗

Endothelial dysfunction in cold-induced hypertensive rats.

Endothelial dysfunction can be observed in preatherosclerotic conditions. However, its pathogenetic role in hypertension is still controversial. Endothelial-dependent changes of blood pressure (BP) and expression of endothelial nitric oxide synthase (eNOS) were evaluated in cold-induced hypertensive rats. Wistar rats were exposed to cold stress for 8 weeks. Exposure to cold stress significantly increased the systolic BP in rats. The infusion of acetylcholine significantly lowered mean arterial BP in control rats by 48 +/- 2% and by 32 +/- 1% in cold-induced hypertensive rats. The acetylcholine-induced reduction of mean arterial BP was significantly attenuated in cold-induced hypertensive rats (control rats, 45 +/- 2 mm Hg; cold-induced hypertensive rats, 34 +/- 3 mm Hg; P < .05). Administration of N(G)-nitro-L-arginine-methyl ester for 1 week significantly increased BP in control rats, whereas no effect could be observed in cold-induced hypertensive rats. In cold-induced hypertensive rats eNOS in aortic vessels was significantly reduced compared to control rats. In this nongenetic, nonsurgical animal model of cold-induced hypertensive rats an endothelial dysfunction can be observed due to reduced eNOS.

Acetylcholine↗

Cold acclimation-induced increase of systolic blood pressure in rats is associated with volume expansion.

To investigate the mechanisms of cold-induced hypertension, the systolic blood pressure (SBP) and average daily water consumption were measured weekly in 6-month-old male Wistar rats; they were subsequently acclimated to thermoneutrality (26 degrees C for 7 weeks), to cold temperature (6 degrees C for 9 weeks), and then again reacclimated to 26 degrees C for 5 weeks. Circulating plasma volume and whole blood viscosity were measured in subgroups of rats at the end of acclimation to 26 degrees C after 2 days, after 1, 6, and 8 weeks of cold, and after 2 and 5 weeks of rewarming. The control values obtained at the end of thermoneutral period were: SBP = 130.8 +/- 18.6 mm Hg, plasma volume = 41.9 +/- 4.64 mL/kg, whole body viscosity at shear rate of 22.5 per sec = 6.7 +/- 0.48 cps, and daily water consumption = 42.25 +/- 16.81 mL. After 48 h of cold exposure there was almost a 50% increase in plasma volume that persisted to a lesser degree throughout the whole period of cold exposure (P < .05). After 2 weeks of cold exposure the daily water consumption increased and SBP began to increase. After 6 weeks of cold exposure the SBP was 30 mm Hg above that of the control level (P < .001) and was accompanied by a 25% increase in whole blood viscosity (P < .05). At the end of 8 weeks of cold exposure the plasma volume was 56.8 +/- 9.51 mL/ kg and the whole blood viscosity was 8.0 +/- 1.79 cps at the 22.5 per sec shear rate. During the 5 weeks of rewarming the elevation of SBP and increased whole blood viscosity persisted, whereas the increased daily water consumption and expanded plasma volume returned to normal. Therefore, the acclimation to cold is accompanied by the development of a volume-associated hypertension, which is sustained after rewarming without volume expansion.

Acclimatization↗

Stearic acid oxidation in the Alaskan red-backed vole: effects of cold and norepinephrine.

Saturated fatty acids constitute a considerable energy reserve that could convey survival value under chronic cold exposure. It was investigated whether acclimation to cold was associated with a change in the ability of a small microtine rodent, the red-backed vole (Clethrionomys rutilis), to increase the use of saturated fatty acids during thermogenesis. The C-14 labeled stearic acid, a typical saturated fatty acid (FA), was used to determine the rate of utilization through oxidation. In warm acclimated (WA, 20 degrees C) and cold acclimated (CA, 5 degrees C) voles, acute cold exposure (WA at 5 degrees C, -2 degrees; CA at -5 degrees C) and norepinephrine (NE) injection increased metabolic rate (VO2, VCO2) and mobilization of lipid reserves. Acute cold exposure increased percent blood stearate oxidized in a linear fashion with both metabolic rate and stearate concentration in both WA and CA voles. The CA voles at 5 degrees C had increased stearate irreversible loss (1.5x) and oxidation rate (2x) compared to WA voles at 20 degrees C. The CA voles at -5 degrees C increased stearate irreversible loss and oxidation linearly with metabolic rate and blood stearate concentration. In CA voles the contribution made by stearate oxidation to VCO2, increased with the level of cold exposure and NE injection. In contrast, for WA voles stearate irreversible loss and the contribution made by stearate oxidation to VCO2 were unaffected by acute cold exposure. Thus, cold acclimation involves: (1) a modest increase (1.5x) in the use of stearate as a fuel substrate; and (2) a greater stearate oxidation and contribution to overall metabolism during acute cold exposure (-5 degrees C).

Acclimatization↗

Hairpin folding dynamics: the cold-denatured state is predisposed for rapid refolding.

Cold denaturation is a general phenomenon in globular proteins, and the associated cold-denatured states of proteins have important fundamental and practical significance. Here, we have characterized the cold-denatured state of a beta-hairpin forming peptide, MrH3a, in 8% hexafluoro-2-propanol (HFIP) and the dynamics of its refolding following a laser-induced T-jump. Beta-hairpins constitute an important class of protein structural elements, yet their folding mechanisms are not fully understood. Characterization of MrH3a using NMR, CD, and IR spectroscopies reveals residual structure in the cold-denatured state, in contrast with the highly disordered heat-denatured state. The residual structure in the cold-denatured state comprises relatively compact and solvent protected conformations. Furthermore, we find a substantial acceleration in the rate of folding from the cold-denatured state compared to that of the heat-denatured state. In addition, the cold-denatured state is not populated in 20% HFIP; folding occurs only from the fully unfolded state and is significantly slower. We interpret the acceleration of the folding rate of MrH3a in 8% HFIP as a direct consequence of the collapsed conformations of the cold-denatured state. Finally, there may be some reduction of the loop search cost when starting from the cold-denatured state, since this state may have some of the stabilizing cross-strand interactions already formed.

Circular Dichroism↗

Influence of nucleotides on the cold stability of chloroplast coupling factor 1.

Chloroplast coupling factor 1 (CF1), a cold-labile enzyme, contains six nucleotide binding sites. These sites are located at the alpha/beta interfaces of the alpha 3 beta 3 heterohexamer. The cold lability of CF1 is decreased by the presence of nucleotides in the medium. We have studied the influence of both different nucleotides and different binding sites on the cold dissociation of CF1. To monitor the dissociation of CF1 during cold treatment, 8-anilino-1-naphthalenesulfonic acid (ANS) was employed. The increase in ANS fluorescence during cold treatment is the result of increased accessibility of intersubunit hydrophobic regions as the complex dissociates. Mg(2+)-adenosine triphosphates, tightly bound to CF1, markedly stabilize the enzyme in the cold. ADP only protects CF1 from dissociating in the cold when it is bound to the loose sites or when it is bound in conjunction with Mg2+. CF1 that contained 2 mol of ADP/mol and little bound Mg2+ was nearly as cold labile as CF1 that contained just 0.2 mol of ADP/mol. When about one of the two bound ADPs was replaced with adenylyl beta, gamma-imidodiphosphate (AMP-PNP), some protection from cold dissociation was observed. These results show that the site(s) occupied, as well as the nucleotides they contain, strongly influence(s) the structural stability of CF1.

Adenosine Diphosphate↗

Verapamil improves the response of coronary vasomotion to cold pressor test in asymptomatic and mildly symptomatic patients with hypertrophic cardiomyopathy.

Impaired endothelium-dependent vasodilatation of coronary resistance vessels was previously demonstrated in patients with hypertrophic cardiomyopathy (HC). Therefore, we decided to assess the effect of verapamil administration on the response of diastolic coronary blood flow velocity (CBFV) and the coronary vascular resistance index to the cold pressor test in asymptomatic and mildly symptomatic HC patients. In 10 patients with nonobstructive HC, the CBFV was detected in the distal portion of the left anterior descending coronary artery using high-sensitivity transthoracic Doppler echocardiography. Peak diastolic CBFV, the velocity-time integral of diastolic CBF, and the coronary vascular resistance index (calculated as the mean aortic pressure/CBFV ratio) were measured at baseline and after the cold pressor test. The percentage changes from baseline to the cold pressor test of these parameters were compared before and after 1 month of verapamil therapy. Open-label verapamil changed the decrease in CBFV into an increase in response to the cold pressor test (from -4.1 +/- 6.4% to +11 +/- 10.9%, P < 0.01). A similar reversibility of changes in the velocity-time integral of CBF in response to the cold pressor test after verapamil therapy was observed (from -3.3 +/- 8.3% to +9.6 +/- 10.3%, P < 0.05). Verapamil reversed the response of coronary resistance vessels to the cold pressor test from a +12 +/- 9.8% increase to a -5.2 +/- 10.2% decrease in the coronary vascular resistance index (P < 0.01). We concluded that in asymptomatic and mildly symptomatic HC patients in response to the cold pressor test, treatment with open-label verapamil increased CBF parameters and decreased the coronary vascular resistance index. Verapamil reversed the abnormal vasoconstrictor to vasodilator response of coronary resistance vessels to the cold pressor test. The restoration of the vasodilator response to the cold pressor test by verapamil suggests the potential positive effect of verapamil on endothelium-dependent coronary vasodilation in HC patients. Thus, a randomized blinded trial is now required.

Adult↗

Metabolic changes induced by cold stress in rat liver mitochondria.

The mechanisms involved in the metabolic changes induced by cold stress in isolated rat liver mitochondria were studied. Respiration, ATP synthesis, and membrane potential as well as the contents of several metabolites were determined in liver mitochondria from cold-exposed rats. At different times of cold exposure, the force-flux relationships showed net variation in flux (enhanced respiration, diminished ATP synthesis) with no associated variation in force (H+ gradient); this suggested that decoupling rather than classical uncoupling was involved in the effects of cold stress. The flux control coefficient of the H+ leak on basal respiration was slightly increased by 380 h of cold exposure. Cold stress also induced a diminution in total membrane fatty acids, Zn2+, Fe3+, ATP, and ADP/O ratios; the content of cytochromes c + c1 and b oscillated. The contents of Ca2+, Na+, Pi, and cytochromes a + a3 were not affected, whereas matrix ADP, AMP, K+, and Mg2+ were markedly increased. Basal and oleic acid-stimulated respiration of mitochondria from cold-stressed rats was inhibited by GDP, carboxyatractyloside, or albumin. These agents did not affect basal respiration in control mitochondria. Western blot analysis showed enhanced expression of a protein of about 35 kDa, presumably the uncoupling protein 2, induced by long-term cold exposure. The overall data suggest that cold stress promoted decoupling of oxidative phosphorylation, and hence, changes in several matrix metabolites, by increasing free fatty acids and the UCP2 content.

Adenine Nucleotides↗

Topology of EEG coherence changes may reflect differential neural network activation in cold and pain perception.

Pain perception in the brain can be analyzed by neuroimaging (PET, fMRI) and electrophysiological parameter mapping (EEG, ERP/MEG, MEF). These studies have generally been focused on the localization of cerebral activation. Whether pain can be conceptualized as localized function or best be understood by distributed function is important to the theory of human pain processing in the brain. Here, we report that cold and pain perception in the brain is characterized by webs of EEG coherence changes which may reflect coupling or de-coupling of different cortical areas during cold and pain processing. EEG was recorded during cold and pain perception (right hand immersion in 15 degrees C cool-water vs. 0.3 degrees C ice-water for 3 min.) with eyes opened. Subjects rated the cold perception at 2.3 (cool to cold, but no pain) and the pain perception at 6.7 (moderate-strong pain) in a 1-10 scale. The obtained EEG spectral parameters were compared with the corresponding parameters of the resting baseline using paired Wilcoxon tests in the sense of statistical filters to depict those differences which differ clearly from changes by chance. The results were presented in probability maps. The EEG results indicated highly differential coherence networks between cold and pain perception. The cold perception was characterized as decreased coherence in the theta band mainly between frontal electrodes and increased interhemispheric coherence in the alpha range mainly between central and frontal positions. During pain perception almost no coherence changes in the theta band were observed, but great coherence increase in the delta band between central, parietal and frontal electrodes. The network of coherence changes in the alpha band showed strong involvement of electrode C3 concerning coherence increases with frontal positions. In the beta-1 band coherence increase within the left hemisphere was much more pronounced during pain than during cold. The differential characteristics of EEG coherence changes based on neural networks and their spatial organization in the neocortex indicate the distributed brain processing between cold and pain perception in man. This study may contribute to our understanding of the large scale neural networks in cognition based on neurophysiological binding hypothesis and network connections of neural ensembles.

Adult↗

Vinegar dressing and cold storage of potatoes lowers postprandial glycaemic and insulinaemic responses in healthy subjects.

OBJECTIVE: To investigate the effects of cold storage and vinegar addition on glycaemic and insulinaemic responses to a potato meal in healthy subjects. SUBJECTS AND SETTING: A total of 13 healthy subjects volunteered for the study, and the tests were performed at Applied Nutrition and Food Chemistry, Lund University, Sweden. Experimental design and test meals:The study included four meals; freshly boiled potatoes, boiled and cold stored potatoes (8 degrees C, 24 h), boiled and cold stored potatoes (8 degrees C, 24 h) with addition of vinaigrette sauce (8 g olive oil and 28 g white vinegar (6% acetic acid)) and white wheat bread as reference. All meals contained 50 g available carbohydrates and were served as a breakfast in random order after an overnight fast. Capillary blood samples were collected at time intervals during 120 min for analysis of blood glucose and serum insulin. Glycaemic (GI) and insulinaemic indices (II) were calculated from the incremental areas using white bread as reference. RESULTS: Cold storage of boiled potatoes increased resistant starch (RS) content significantly from 3.3 to 5.2% (starch basis). GI and II of cold potatoes added with vinegar (GI/II=96/128) were significantly reduced by 43 and 31%, respectively, compared with GI/II of freshly boiled potatoes (168/185). Furthermore, cold storage per se lowered II with 28% compared with the corresponding value for freshly boiled potatoes. CONCLUSION: Cold storage of boiled potatoes generated appreciable amounts of RS. Cold storage and addition of vinegar reduced acute glycaemia and insulinaemia in healthy subjects after a potato meal. The results show that the high glycaemic and insulinaemic features commonly associated with potato meals can be reduced by use of vinegar dressing and/or by serving cold potato products.

Acetic Acid↗