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PubMed2004

Cold-induced hyperthyroidism produces oxidative damage in rat tissues and increases susceptibility to oxidants.

In this work, we investigated whether cold exposure-induced hyperthyroidism increases oxidative damage and susceptibility to oxidants of rat liver, heart and skeletal muscle. All tissues exhibited gradual increases in hydroperoxide and protein-bound carbonyl levels. Glutathione peroxidase activity increased in all tissues after 2 days and further increased in the muscle after 10 days of cold exposure. Liver glutathione reductase activity increased after 10 days of cold exposure, while heart and muscle activities were not modified. Vitamin E levels were not affected by cold, while coenzyme Q9 and coenzyme Q10 levels decreased in heart and muscle after 2-day cold exposure and were not further modified after 10 days. Liver coenzyme Q9 levels increased after 2 days whereas coenzyme Q10 levels increased after 10 days in the cold. The whole antioxidant capacity was lowered, while parameters positively correlated with susceptibility to oxidants were increased by cold. Lipid fatty acid composition was modified in all tissues. In particular, fatty acid unsaturation degree increased in heart and muscle. Cytochrome oxidase activity increased, suggesting an increased content of hemoproteins, which are able to generate .OH radical. This view was supported by the observation that the tissue susceptibility to H(2)O(2) treatment, which is strongly correlated to iron-ligand content, increased after cold exposure. In this frame, it is apparent that the increase in oxidative capacity, necessary for homeotherm survival in low temperature environments, has potential harmful effects, because it results in increased susceptibility to oxidative challenge.

Animals↗
PubMed2004

Seasonal changes in thermal responses of urban residents to cold exposure.

To determine whether urban circumpolar residents show seasonal acclimatisation to cold, thermoregulatory responses and thermal perception during cold exposure were examined in young men during January-March (n=7) and August-September (n=8). Subjects were exposed for 24 h to 22 and to 10 degrees C. Rectal (T(rect)) and skin temperatures were measured throughout the exposure. Oxygen consumption (VO(2)), finger skin blood flow (Q(f)), shivering and cold (CDT) and warm detection thresholds (WDT) were assessed four times during the exposure. Ratings of thermal sensations, comfort and tolerance were recorded using subjective judgement scales at 1-h intervals. During winter, subjects had a significantly higher mean skin temperature at both 22 and 10 degrees C compared with summer. However, skin temperatures decreased more at 10 degrees C in winter and remained higher only in the trunk. Finger skin temperature was higher at 22 degrees C, but lower at 10 degrees C in the winter suggesting an enhanced cold-induced vasoconstriction. Similarly, Q(f) decreased more in winter. The cold detection threshold of the hand was shifted to a lower level in the cold, and more substantially in the winter, which was related to lower skin temperatures in winter. Thermal sensations showed only slight seasonal variation. The observed seasonal differences in thermal responses suggest increased preservation of heat especially in the peripheral areas in winter. Blunted vasomotor and skin temperature responses, which are typical for habituation to cold, were not observed in winter. Instead, the responses in winter resemble aggravated reactions of non-cold acclimatised subjects.

Adult↗
PubMed2006

Antisense knock down of TRPA1, but not TRPM8, alleviates cold hyperalgesia after spinal nerve ligation in rats.

Patients with neuropathic pain frequently experience hypersensitivity to cold stimulation. However, the underlying mechanisms of this enhanced sensitivity to cold are not well understood. After partial nerve injury, the transient receptor potential ion channel TRPV1 increases in the intact small dorsal root ganglion (DRG) neurons in several neuropathic pain models. In the present study, we precisely examined the incidence of cold hyperalgesia and the changes of TRPA1 and TRPM8 expression in the L4 and L5 DRG following L5 spinal nerve ligation (SNL), because it is likely that the activation of two distinct populations of TRPA1- and TRPM8-expressing small neurons underlie the sensation of cold. We first confirmed that L5 SNL rats developed cold hyperalgesia for more than 14 days after surgery. In the nearby uninjured L4 DRG, TRPA1 mRNA expression increased in trkA-expressing small-to-medium diameter neurons from the 1st to 14th day after the L5 SNL. This upregulation corresponded well with the development and maintenance of nerve injury-induced cold hyperalgesia of the hind paw. In contrast, there was no change in the expression of the TRPM8 mRNA/protein in the L4 DRG throughout the 2-week time course of the experiment. In the injured L5 DRG, on the other hand, both TRPA1 and TRPM8 expression decreased over 2 weeks after ligation. Furthermore, intrathecal administration of TRPA1, but not TRPM8, antisense oligodeoxynucleotide suppressed the L5 SNL-induced cold hyperalgesia. Our data suggest that increased TRPA1 in uninjured primary afferent neurons may contribute to the exaggerated response to cold observed in the neuropathic pain model.

Animals↗
PubMed2004

Susceptibility of Vibrio parahaemolyticus to various environmental stresses after cold shock treatment.

Vibrio parahaemolyticus was subjected to cold shock treatment at 20 or 15 degrees C for 2 or 4 h. The effect of cold shock on the survival of V. parahaemolyticus subjected to subsequent low temperature (5 and -18 degrees C) and other adverse conditions (47 degrees C, 6 ppm crystal violet, 1000 ppm H(2)O(2), 25 mM acetic acid and 25 mM lactic acid) was investigated. Regardless of the cold shock treatment, survival of V. parahaemolyticus increased when stored at 5 or -18 degrees C, while no increase in survival was noted for cells cold shocked in the presence of chloramphenicol. Cold shock treatment under the conditions tested, in general, enabled V. parahaemolyticus cells to survive better following subsequent challenge by crystal violet, while the cold-shocked organism was more susceptible to high temperature (47 degrees C), H(2)O(2) and organic acids (lactic and acetic acid) than the non-shocked cells. Furthermore, the temperature and time of the cold shock treatment affected the cold shock response of V. parahaemolyticus.

Acetic Acid↗
PubMed2006

Plasma membrane lipid alterations induced by cold acclimation and abscisic acid treatment of winter wheat seedlings differing in frost resistance.

Cold acclimation of plants affects many aspects of metabolism. Changes in plasma membrane lipids have always been considered to be important for development of frost resistance and survival at subzero temperatures. We studied different cultivars of winter wheat (Triticum aestivum L.) that differed in frost resistance induced either by cold acclimation or treatment with the plant hormone abscisic acid (ABA). Plasma membranes were isolated from non-acclimated and cold- as well as from ABA-acclimated plants, and were subjected to detailed lipid analysis. Cold acclimation affected virtually all plasma membrane lipid components and their constituents, resulting in both increases and decreases, which varied between the three groups of plants investigated. Including the cold-induced variations observed in the few plant species studied in detail previously, cerebrosides were the only components reduced by cold acclimation in all plants. In wheat, more uniform and consistent patterns were obtained when considering colligative parameters such as total free sterols, phospholipids or glycolipids, either as the proportion of total lipids or based on plasma membrane protein. The parameter which changed most significantly in parallel to the increase of inducible frost resistance in the three groups of plants was the ratio of free sterols/glycolipids, which increased. ABA treatment resulted in qualitatively similar effects in only one cultivar, but in general these changes were less pronounced. Compared to changes in transcription rates of several cold-induced genes and in the concentration of various compatible solutes reported for other plants, the observed changes in plasma membrane lipids are minor ones. This may indicate that acclimation-induced changes can be accomplished by posttranscriptional regulation of enzymatic activities, which is in agreement with the failure to detect significant changes in transcription of the corresponding genes during cold induction.

Abscisic Acid↗
PubMed2004

Noxious heat receptors present in cold-sensory cells in rats.

Noxious heat above approximately 45 degrees C applied on cold spots evokes a paradoxical cold sensation by activating cold fibers. It remains unresolved whether cold receptors respond to heat as well, or whether noxious-heat receptors and cold receptors coexist in the same fiber. Recently, noxious heat receptors (TRPV1) and cold receptors (TRPM8) have been cloned. It is controversial, however, whether TRPV1 and TRPM8 coexist in the same sensory neuron. Here, we investigate colocalization of these receptors in dorsal root ganglion (DRG) of rats. TRPV1 was expressed in 29% of TRPM8-positive cells in DRG sections. In Ca2+ imaging, noxious heat excited many of the cold-sensitive cells in culture. In a whole-cell current-clamp mode, noxious heat, capsaicin, cooling and menthol all evoked receptor potentials and impulses in a subset of DRG neurons. This colocalization of TRPV1 and TRPM8 in a DRG neuron may be the basis for the paradoxical cold sensation.

Animals↗
PubMed1996

Comparison between positron emission tomography myocardial perfusion imaging and intracoronary Doppler flow velocity measurements at rest and during cold pressor testing in angiographically normal coronary arteries in patients with one-vessel coronary artery disease.

With use of invasive methods, coronary endothelial function is generally studied by examining the response of epicardial coronary arteries to intracoronary administered acetylcholine or to cold pressor testing. Because invasive methods have substantial inherent limitations, studies should attempt to evaluate coronary endothelial function noninvasively. This study examines a noninvasive technique for endothelium-related coronary stress testing. In myocardial regions supplied by nonstenotic coronary arteries, we compared positron emission tomography (PET) myocardial perfusion imaging with intracoronary Doppler flow velocity measurements during endothelium-related stress testing. PET perfusion was examined at rest and during cold pressor testing in 10 patients with 1-vessel coronary artery disease. In nonstenotic coronary arteries, flow velocity measurements were obtained at rest, during cold pressor testing, and during intracoronary administered acetylcholine. Perfusion and flow velocity responses and stress/rest ratios were compared between the techniques during the various circumstances. Positive correlations were found between: (1) cold pressor Doppler flow velocity responses and acetylcholine Doppler flow velocity responses (r = 0.84, SEE = 0.19, p = 0.003); (2) cold pressor PET perfusion responses and cold pressor Doppler flow velocity responses (r = 0.70, SEE = 0.17, p = 0.02); and (3) cold pressor PET perfusion responses and acetylcholine Doppler flow velocity responses (r = 0.62, SEE = 0.19, p = 0.05). These results suggest that in angiographically normal coronary arteries, both the flow velocity and the perfusion responses during cold pressor testing may be related to the response to acetylcholine.

Acetylcholine↗
PubMed1999

Effect of intravenous infusion of a beta-adrenergic blocking agent on the haemodynamic changes in human masseter muscle induced by cold-pressor stimulation.

Eight healthy non-smoking males (mean age: 24.1 +/- 1.1 years) without any history of chronic muscle pain and migraine participated in this study. Haemoglobin (Hb) and oxygen (O2) saturation in the right masseter muscle were continuously recorded with a non-invasive near-infrared spectroscopic device. Heart rate and blood pressure were also recorded. The experiment had three phases: a placebo drug (physiological saline) with cold-pressor trial, a 30-sec maximal voluntary clenching (MVC) trial, and a propranolol with cold-pressor trial. The saline and drug trials each involved continuous recording for 1 min before, 2 min during and 5 min after the cold-pressor stimulation (4 degrees C). Physiological saline (20 ml) or propranolol hydrochloride (20 ml) were infused at the rate of 2 ml/min. This infusion was begun 20 min before the baseline recording and participants did not know which solution (saline or propranolol) was being infused. For the MVC trial, each participant was asked to perform a 30-sec clench of their jaw-closing muscles. There was a rest period of 15 min between each trial. The individual Hb and O2 data were normalized so that the baseline at the beginning of the experiment was equal to zero, and the Hb and O2 data were normalized as a percentage of the individual's own highest absolute Hb and O2 after and during the MVC, respectively. The results showed that the mean baseline Hb 1 min before cold-pressor stimulation was significantly lower in the beta-blocker trial than in the placebo trial (p = 0.035). The mean change in Hb from baseline during cold-pressor stimulation in the beta-blocker trial was also significantly less than in the placebo trial (p = 0.035). The mean Hb rebound change after the cold-pressor stimulation in the beta-blocker trial was significantly higher than in the placebo trial, and no significant heart-rate differences were observed in the period after cold-pressor stimulation. Overall, the mean heart rate before and during that stimulation was significantly lower in the beta-blocker trial than the placebo trial (p < 0.001). There was no significant mean blood-pressure difference between placebo and beta-blocker trials at any time. These results suggest that beta-adrenoceptor blocking decreases the blood volume in the resting masseter, suppresses the incremental blood-volume change during cold-pressor stimulation, and discloses a hidden vasoconstrictive effect after that stimulation.

Adrenergic beta-Antagonists↗
PubMed2003

Altered ATP-dependent mitochondrial Ca2+ uptake in cold ischemia is attenuated by ruthenium red.

BACKGROUND: Graft dysfunction as a result of preservation injury remains a major clinical problem in liver transplantation. This is related in part to accumulation of mitochondrial calcium (Ca(2+)), which has been linked to activation of proapoptotic factors. We hypothesized that cold ischemia increases mitochondrial Ca(2+) uptake in a concentration dependent fashion and that ruthenium red (RR) will attenuate these changes by inhibiting the mitochondrial Ca(2+) uniporter. METHODS: Rat livers perfused with cold University of Wisconsin (UW) solution (4 degrees C) with or without RR (10 microM) via the portal vein (n = 3 per group) were processed immediately (no ischemia) or after 24 h cold-storage (24 h cold ischemia). Mitochondria were separated by differential centrifugation, and adenosine triphosphate (ATP)-dependent (45)Ca(2+) uptake was determined in the presence of ATP (5 mM), adenosine diphosphate (ADP), or adenosine 5'-beta,gamma-imidotriphosphate (AMP-PNP); variable concentrations of extramitochondrial (45)Ca(2+) were used. All measurements were performed in triplicate. Student's t test with P < 0.05 was taken as significant. RESULTS: Our data demonstrate the following: 1) ATP-dependent (45)Ca(2+) uptake in mitochondria separated from livers following 24 h of cold ischemia in UW alone was higher than in mitochondria isolated from non-ischemic livers; the increased uptake was dependent on the concentration of (45)Ca(2+) in the incubation buffer. 2) There was no difference in ATP-dependent (45)Ca(2+) uptake between nonischemic mitochondria and those separated from livers stored in UW-RR for 24 h. 3) (45)Ca(2+) uptake in mitochondria from livers subjected to 24 h of cold ischemia in UW-RR was significantly lower compared to those from livers stored in UW alone when (45)Ca(2+) concentrations were greater than 1 microM. CONCLUSION: 1) Cold ischemia affects mitochondrial Ca(2+) handling, especially when it is challenged by high extramitochondrial Ca(2+) concentrations. 2) The addition of RR in preservation solution attenuates the effects of cold ischemia on mitochondrial Ca(2+) handling. 3) Inhibition of mitochondrial Ca(2+) uniporter with RR protects mitochondria from Ca(2+) overload at high Ca(2+) concentrations. These findings may offer a potentially effective strategy for prevention of ischemia-reperfusion injury in liver transplantation.

Adenosine Triphosphate↗
PubMed1997

Varietal differences in protein phosphorylation during cold treatment of rice leaves.

The effects of cold stress on protein phosphorylation in leaves of rice (Oryza sativa) seedlings were investigated. Two-week-old rice seedlings were exposed to low temperature (5 degrees) for 6 hr at a relative humidity of 100%. The leaf protein extracts were phosphorylated in vitro. Cold stress stimulated the phosphorylation of a 60 kDa protein in the cold-sensitive rice variety, IR36. In the cold-tolerant rice variety, Kitaibuki, this protein had already been phosphorylated. For greater clarificating of these changes, the effects of cold on rice varieties differing in cold susceptibility were examined. Cold-sensitive rice varieties showed similar the protein phosphorylation in contrast to the cold-tolerant rice varieties.

Cold Temperature↗
PubMed1998

Sinusitis in the common cold.

BACKGROUND: Acute community-acquired sinusitis is considered a bacterial complication of the common cold. Radiologic abnormalities in sinuses occur, however, in most patients with upper respiratory virus infections. OBJECTIVE: Assessment of the occurrence, clinical profile, laboratory findings, and outcome of radiologically confirmed sinusitis was carried out as part of a common cold study in young adults. METHODS: Clinical examinations and radiography of the paranasal sinuses were carried out on days 1, 7, and 21 in 197 patients with the common cold. The symptoms were recorded on diary cards on days 1 to 20. Ten viruses and 5 bacteria were studied as etiologic agents of common cold as reported earlier. Serum C reactive protein concentrations, erythrocyte sedimentation rates, and total white blood cell counts with differentials were determined in 40 randomized subjects on day 7. The effect of 6 days of intranasal fluticasone propionate treatment of the common cold in the prevention of sinusitis was analyzed. RESULTS: On day 7, 39% of patients with the common cold in the placebo group (n = 98) had sinusitis, which we would prefer to call viral sinusitis. The symptoms of patients with sinusitis and those without it were not clinically distinguishable. Viral infection was detected in 81.6% of patients with sinusitis. No significantly increased levels of antibodies to bacteria were detected. Serum C reactive protein concentrations, erythrocyte sedimentation rates, and white blood cell counts were low in patients with sinusitis. All patients made a clinical recovery within 21 days without antibiotic treatment. Fluticasone propionate treatment tended to prevent paranasal sinusitis, especially in rhinovirus-positive subjects. CONCLUSION: Viral sinusitis frequently occurs in the early days of the common cold, but it is a self-limited illness. The sinuses should not be imaged in patients with the common cold if the signs and symptoms of illness gradually become less severe and no specific signs suggestive of bacterial sinusitis occur.

Adult↗
PubMed1985

Cold urticaria. Clinical findings in 220 patients.

Patients with cold urticaria, a total of 220, were studied in Finland. Sixty-three percent of the patients were female. The diagnosis was based on a positive ice cube test in 90% of cases, and the other cold tests were needed to certify the diagnosis for the remainder of patients. The mean age at the onset of the disease was 25.1 years (range, 1-74), and the mean duration of symptoms was 6.3 years (range, 3 weeks to 37 years). Cold urticaria symptoms had disappeared in fifty-three patients (24%), but there was a recurrence of the disease in twelve. Idiopathic (primary acquired) cold urticaria was present in 96% of the patients. Only two patients had a secondary acquired cold urticaria. Two patients had cold-induced, "cholinergic" urticaria, and four patients had a delayed type of cold urticaria. Twenty-one percent of the patients had dermatographism, 8% had cholinergic urticaria, and two patients (1%) had heat urticaria concurrently with cold urticaria.

Adolescent↗
PubMed1997

Role of hypothalamic neuropeptide Y neurons in the defective thermogenic response to acute cold exposure in fatty Zucker rats.

The fatty Zucker rat has impaired heat production and fails to mount an adequate thermogenic response to cold exposure, partly because of decreased sympathetic drive to thermogenesis in brown adipose tissue. Neuropeptide Y, synthesized in neurons of the hypothalamic arcuate nucleus and released in the paraventricular nucleus, stimulates feeding and inhibits brown adipose tissue activity. The neuropeptide Y neurons are overactive in fatty Zucker rats and are thought to contribute to hyperphagia, reduced energy expenditure and obesity. We have examined the relationship between thermogenic activity in brown adipose tissue (measured as uncoupling protein messenger RNA levels) and hypothalamic neuropeptide Y and neuropeptide Y messenger RNA levels in response to cold exposure (4 degrees C) for 2.5 and 18 h, in fatty and lean Zucker rats. In lean Zucker rats, cold exposure at 4 degrees C for 2.5 and 18 h significantly increased uncoupling protein messenger RNA levels by 3.5-fold (P<0.01) and 3.3-fold (P<0.01), respectively, compared with warm-maintained controls. Exposure to cold for 18 h also increased neuropeptide Y concentrations in the paraventricular nucleus (P<0.01) and ventromedial nucleus (P<0.001) in lean rats, with no change in neuropeptide Y messenger RNA after either 2.5 or 18 h. By contrast, fatty Zucker rats showed no significant changes in uncoupling protein messenger RNA (P>0.05) at either duration of cold exposure. There were also no significant changes in neuropeptide Y levels in any region nor in neuropeptide Y messenger RNA, with cold exposure for either period (P>0.05). In lean rats, cold exposure therefore stimulates brown fat uncoupling protein messenger RNA and also increases neuropeptide Y concentrations in its hypothalamic sites of release. We suggest that increased brown fat thermogenic capacity induced by cold in lean rats may be mediated, at least in part, by decreased neuropeptide Y release in the paraventricular nucleus, resulting in its accumulation in this site. Defective thermogenic responses in fatty rats may result from central dysregulation of brown adipose tissue due to sustained and non-suppressible overactivity of hypothalamic neuropeptide Y neurons.

Animals↗
PubMed1999

Early decrease in apurinic/apyrimidinic endonuclease is followed by DNA fragmentation after cold injury-induced brain trauma in mice.

Apurinic/apyrimidinic endonuclease, a multifunctional protein in the DNA base excision repair pathway, plays a central role in repairing DNA damage caused by reactive oxygen species. We examined protein expression of apurinic/apyrimidinic endonuclease before and after cold injury-induced brain trauma in mice, where we have previously shown reactive oxygen species to participate. Immunohistochemistry showed the nuclear expression of apurinic/apyrimidinic endonuclease in the entire region of control brains. One hour after cold injury-induced brain trauma, nuclear immunoreactivity was predominantly decreased in the inner boundary of the lesion, whereas there was a slight increase in the outer boundary area. Four hours after cold injury-induced brain trauma, nuclear immunoreactivity was almost absent in the entire lesion, and remained so until 24 h. At this time, a marked increase in apurinic/apyrimidinic endonuclease immunoreactivity was seen in the outer boundary zone. Western blot analysis of the sample from the non-ischemic area showed a characteristic 37,000 mol. wt band, which decreased markedly 24 h after cold injury-induced brain trauma. A time-dependent increase in DNA fragmentation was also observed after cold injury-induced brain trauma. Our data provide the first evidence that apurinic/apyrimidinic endonuclease decreased rapidly in the lesion after cold injury-induced brain trauma, whereas it was significantly increased at the outer boundary zone. Although further examination is necessary to elucidate the direct relationship between apurinic/apyrimidinic endonuclease alteration and the pathogenesis of cold injury-induced brain trauma, our results suggest the possibility that an early decrease in apurinic/apyrimidinic endonuclease and failure of the DNA repair mechanism may contribute to DNA-damaged neuronal cell death after cold injury-induced brain trauma.

Animals↗
PubMed1996

Long-term follow-up evaluation of cold sensitivity following nerve injury.

This article reports the long-term follow-up evaluation (mean, 10 years) findings of 50 patients with upper-extremity peripheral nerve injuries. The most common persistent symptom was cold sensitivity (n = 38), and 33 of 38 patients rated its intensity as moderate or severe. Cold sensitivity typically developed within months after initial injury and resolved in only 2 patients. No significant difference in the incidence of cold sensitivity was found between patients with subjectively normal hand sensation (7 of 11) and those who reported abnormal hand sensibility (31 of 37). A cold sensitivity severity score (CSSS) was determined; a significant relationship was found between the CSSS and the patient's subjective rating of cold sensitivity intensity and change in job status or occupation due to injury (p < or = .02). No significant relationships were found between incidence of cold sensitivity and age, mechanism of injury, smoking, or level of nerve injury. A significant relationship was found between cold sensitivity and digital amputation injuries (p < or = .05). Thus, cold sensitivity is a common sequela following nerve injury and does not decrease over time.

Adult↗
PubMedDate not supplied

Change in heat loss as a part of adaptation to repeated cold exposures in adult and aged male C57BL/6J mice.

Previous studies have shown that adult mice increase cold-induced heat production as a result of repeated exposures to cold, but that aged mice do not. The objective of the present study was to investigate changes in heat loss during repeated cold exposures in adult and aged C57BL/6J mice. Mice were partially restrained for three hours at 6 degrees C, three times at one-week intervals. Dry heat loss was inferred from measurements of differential temperature between the incoming and outgoing air in the experimental chamber. During the first cold exposure, aged mice showed less heat loss (both total and adjusted for body temperature) than adult animals, suggesting greater peripheral vasoconstriction in aged mice. With repeated cold exposures, both age groups showed increased heat loss, but the aged mice showed greater increase of heat loss, so that by the third cold stress test, no significant differences in heat loss between adult and aged mice were observed. The increase of heat loss after repeated cold exposures in aged mice might reflect a lesser peripheral vasoconstriction, serving to reduce the possibility of tissue necrosis in the cold.

Acclimatization↗
PubMed2001

Effect of hypomagnesemia and cold exposure on tissue responsiveness to insulin in sheep given a low magnesium and high potassium diet.

Hypomagnesemia in ruminants has been shown to be associated with cold stress and with altered insulin secretion and sensitivity. However, the relationship between hypomagnesemia and tissue responsiveness to insulin in ruminants exposed to cold environment is still unclear. The hyperinsulinemic euglycemic clamps, four insulin infusion rates (1, 2, 4 and 8 mU x kgBW(-1) x min(-1) for four sequential periods of 2-h each) were performed to determine combined effects of hypomagnesemia and cold exposure (0 degrees C) on tissue responsiveness to insulin in sheep. The low magnesium (0.05% Mg) and high potassium (4.20% K) diet and cold exposure decreased (P <.05) plasma Mg levels compared with those of the control diet (0.28% Mg/0.52% K) and the thermoneutral environment (20 degrees C). In the euglycemic clamps, cold exposure increased (P <.01) the pooled glucose infusion rate (GIR) across various insulin infusion rates in both diet treatments, though the increases in GIR were small for the low Mg/high K diet. In the cold environment, the GIR was lower (P <.01) for the low Mg/high K diet-fed sheep than for the control diet-fed sheep. The maximal insulin-induced increase in GIR was lower (P <.01) in the hypomagnesemic sheep than in the control sheep during cold exposure, and the insulin level resulting in half-maximal GIR tended to be higher in the hypomagnesemic sheep than in the control sheep. These results indicated that hypomagnesemia in ruminants depressed the enhanced tissue responsiveness to insulin in the cold environment, and decreased insulin-mediated glucose disposal.

Animals↗
PubMed1998

Structural adaptations of the cold-active citrate synthase from an Antarctic bacterium.

BACKGROUND: The structural basis of adaptation of enzymes to low temperature is poorly understood. Dimeric citrate synthase has been used as a model enzyme to study the structural basis of thermostability, the structure of the enzyme from organisms living in habitats at 55 degrees C and 100 degrees C having previously been determined. Here the study is extended to include a citrate synthase from an Antarctic bacterium, allowing us to explore the structural basis of cold activity and thermostability across the whole temperature range over which life is known to exit. RESULTS: We report here the first crystal structure of a cold-active enzyme, citrate synthase, isolated from an Antarctic bacterium, at a resolution of 2.09 A. In comparison with the same enzyme from a hyperthermophilic host, the cold-active enzyme has a much more accessible active site, an unusual electrostatic potential distribution and an increased relative flexibility of the small domain compared to the large domain. Several other features of the cold-active enzyme were also identified: reduced subunit interface interactions with no intersubunit ion-pair networks; loops of increased length carrying more charge and fewer proline residues; an increase in solvent-exposed hydrophobic residues; and an increase in intramolecular ion pairs. CONCLUSIONS: Enzymes from organisms living at the temperature extremes of life need to avoid hot or cold denaturation yet maintain sufficient structural integrity to allow catalytic efficiency. For hyperthermophiles, thermal denaturation of the citrate synthase dimer appears to be resisted by complex networks of ion pairs at the dimer interface, a feature common to other hyperthermophilic proteins. For the cold-active citrate synthase, cold denaturation appears to be resisted by an increase in intramolecular ion pairs compared to the hyperthermophilic enzyme. Catalytic efficiency of the cold-active enzyme appears to be achieved by a more accessible active site and by an increase in the relative flexibility of the small domain compared to the large domain.

Amino Acid Sequence↗