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PubMed2001

Short-term K(+) deprivation provokes insulin resistance of cellular K(+) uptake revealed with the K(+) clamp.

We aimed to test the feasibility of quantifying insulin action on cellular K(+) uptake in vivo in the conscious rat by measuring the exogenous K(+) infusion rate needed to maintain constant plasma K(+) concentration ([K(+)]) during insulin infusion. In this "K(+) clamp" the K(+) infusion rate required to clamp plasma [K(+)] is a measure of insulin action to increase net plasma K(+) disappearance. K(+) infusion rate required to clamp plasma [K(+)] was insulin dose dependent. Renal K(+) excretion was not significantly affected by insulin at a physiological concentration ( approximately 90 microU/ml, P > 0.05), indicating that most of insulin-mediated plasma K(+) disappearance was due to K(+) uptake by extrarenal tissues. In rats deprived of K(+) for 2 days, plasma [K(+)] fell from 4.2 to 3.8 mM, insulin-mediated plasma glucose clearance was normal, but insulin-mediated plasma K(+) disappearance decreased to 20% of control, even though there was no change in muscle Na-K-ATPase activity or expression, which is believed to be the main K(+) uptake route. After 10 days K(+) deprivation, plasma [K(+)] fell to 2.9 mM, insulin-mediated K(+) disappearance decreased to 6% of control (glucose clearance normal), and there were 50% decreases in Na-K-ATPase activity and alpha2-subunit levels. In conclusion, the present study proves the feasibility of the K(+) clamp technique and demonstrates that short-term K(+) deprivation leads to a near complete insulin resistance of cellular K(+) uptake that precedes changes in muscle sodium pump expression.

Animals↗
PubMed2004

Current- and voltage-clamp recordings and computer simulations of Kenyon cells in the honeybee.

The mushroom body of the insect brain is an important locus for olfactory information processing and associative learning. The present study investigated the biophysical properties of Kenyon cells, which form the mushroom body. Current- and voltage-clamp analyses were performed on cultured Kenyon cells from honeybees. Current-clamp analyses indicated that Kenyon cells did not spike spontaneously in vitro. However, spikes could be elicited by current injection in approximately 85% of the cells. Of the cells that produced spikes during a 1-s depolarizing current pulse, approximately 60% exhibited repetitive spiking, whereas the remaining approximately 40% fired a single spike. Cells that spiked repetitively showed little frequency adaptation. However, spikes consistently became broader and smaller during repetitive activity. Voltage-clamp analyses characterized a fast transient Na+ current (INa), a delayed rectifier K+ current (IK,V), and a fast transient K+ current (IK,A). Using the neurosimulator SNNAP, a Hodgkin-Huxley-type model was developed and used to investigate the roles of the different currents during spiking. The model led to the prediction of a slow transient outward current (IK,ST) that was subsequently identified by reevaluating the voltage-clamp data. Simulations indicated that the primary currents that underlie spiking are INa and IK,V, whereas IK,A and IK,ST primarily determined the responsiveness of the model to stimuli such as constant or oscillatory injections of current.

Algorithms↗
PubMed1996

Equivalence of amplified current flowing from dendrite to soma measured by alteration of repetitive firing and by voltage clamp in layer 5 pyramidal neurons.

1. Plots of steady firing rate versus injected current (f-I relations) were constructed from intrasomatic injected current pulses applied alone (control relations) and together with dendritic glutamate iontophoresis (test relations) at sites on the distal apical dendrite 185-555 microns from the soma in layer 5 pyramidal neurons from rat cortex studied in a brain slice. The test f-I relations exhibited a parallel shift along the current axis, and the slopes of the control and test relations differed by < 10% in most neurons. This behavior indicates that constant injected current and steady glutaminergic dendritic input evoke equivalent steady-state repetitive firing in a neuron with active dendrites. The parallel shift of the f-I curves allowed us to compute the amplitude of axial current arriving in the soma from the apical dendrite during repetitive firing. 2. We compared the transmitted current computed from the f-I curve shift with that measured by somatic voltage clamp during the same iontophoresis. When measured during voltage clamp at different somatic membrane potentials, the transmitted current increased with somatic depolarization (was amplified) in most cells, an observation inconsistent with passive dendrites. This larger-amplitude current closely predicted the transmitted current computed from the f-I curve shift, whereas the smaller transmitted current measured at resting potential did not. A set of control experiments indicated that these different predictions were well within the measurement error associated with computation of transmitted current based on f-I curve shifts. The action of blocking agents confirmed that the depolarizing amplification depended on tetrodotoxin (TTX)- and D-2-amino-5-phosphonopentoic acid (APV)-sensitive dendritic channels. 3. The agreement of two independent measurements (somatic voltage clamp and f-I curve shift) of the axial current transmitted from dendrite to soma indicates that the amplification of transmitted current observed in voltage clamp occurs physiologically. We discuss the usefulness of the effective current concept for determining synaptic weighting in network models of neurons with active dendrites.

2-Amino-5-phosphonovalerate↗
PubMed1997

Chorda tympani responses under lingual voltage clamp: implications for NH4 salt taste transduction.

Rat chorda tympani (CT) responses to NH4Cl, ammonium acetate (NH4Ac), and ammonium hippurate (NH4Hp) were obtained during simultaneous current and voltage clamping of the lingual field potential. Although functional and developmental similarities for gustation have been reported for NH4+ and K+ salts, we report here that significant differences are discernible in the CT responses to both salts. Unlike neural responses to KCl, those to NH4Cl are voltage sensitive, enhanced by submucosa negative and suppressed by positive voltage clamp. In this regard, NH4Cl responses are qualitatively similar to NaCl responses; however, the magnitude of NH4Cl voltage sensitivity is significantly less than that of NaCl. The concentration dependence of the CT response to NH4Cl manifests a biphasic nonlinear relationship not observed with KCl or NaCl. Below 0.3 M, the CT response increases as if to approach a saturation value. However, beyond 0.3 M an inflection appears in the CT-concentration curve because of an abrupt increase in CT responses. This kinetic profile is Cl-dependent and is correlated with an increase in transepithelial conductance that displays similar NH4Cl concentration dependence. The biphasic relation to salt concentration is not observed when acetate or hippurate is substituted for Cl-. As with Na+ and K+ salts, less mobile anions than Cl- (Ac- and Hp-) lower the CT responses. However, like Na+ salts, but in contrast to K+ salts, the onset kinetics of CT responses to NH4Ac or NH4Hp remained rapid, even under positive voltage-clamp conditions. Amiloride (100 microM) partially suppresses CT responses within the concentration range of 0.05-0.3 M (48-20% suppression). Amiloride also suppresses the voltage sensitivity of NH4Cl CT responses, but does not eliminate the sensitivity as it does for Na+ salts. In conclusion, the data suggest that taste transduction for NH4 salts is mediated over two NH+ conduction pathways in the taste bud. This is especially evident with NH4Cl, where the CT-concentration curves show two distinct kinetic regimes. Below 0.3 M the saturation with increasing concentration, clamp voltage response dependence, and amiloride sensitivity suggest an apical membrane transduction conductance. Above 0.3 M, the high anion dependence of the response and its amiloride insensitivity indicate participation of the paracellular pathway in transduction.

Amiloride↗
PubMed1999

Patch-clamp-induced perturbations of [Ca(2+)](i) activity in somatotropes.

Somatotropes and GC cells, a GH-producing cell line, exhibit [Ca(2+)](i) oscillations that result from rhythmic Ca(2+) action potentials. Determination of this operating mode required simultaneous recording of both parameters by fura-2 imaging and patch-clamp techniques. In order to test whether patch recording induces artificial alteration of the [Ca(2+)](i) oscillatory pattern, we recorded separately or simultaneously [Ca(2+)](i) and membrane potential. In the absence of any other stimulation, seal formation in patch-clamp recording evoked by itself a 2.5- to 4-fold persistent increase in basal [Ca(2+)](i), speeded up their frequency (from 0.03-0.17 to 0.4 Hz) and changed their pattern to a tonic mode. Patch-induced [Ca(2+)](i) increase was reproduced by mechanical contact between the pipette and the membrane. It was reduced by nifedipine, a blocker of L-type Ca(2+) channels, as well as by removal of external Na(+). It was fully blocked by external Ca(2+) removal or gadolinium. All patch-clamp-induced perturbations were reversed by membrane hyperpolarization. We propose that patch-clamp recording evokes Ca(2+) entry through L-type Ca(2+) channels either directly, or indirectly via membrane depolarization. This shows that patch recordings in endocrine cells showing mechanosensitivity have to be interpreted with caution, and explains why long-lasting patch recordings are so difficult to obtain.

Animals↗
PubMed2001

Modulation of Ca(2+) signaling by microtubule disruption in rat ventricular myocytes and its dependence on the ruptured patch-clamp configuration.

In the absence of hypertrophic proliferation of microtubules, microtubule disruption by colchicine does not modulate contraction of adult cardiac myocytes. However, Gomez et al (Circ Res. 2000;86:30-36) recently reported that disruption of microtubules by colchicine in ruptured patch-clamped myocytes increased I(Ca,L) density and [Ca(2+)](i) transient amplitude and depressed the response of these parameters to the beta-adrenoceptor agonist isoproterenol. These effects were ascribed to stimulation of adenylyl cyclase by increased intracellular free tubulin. In the present study, we show that in intact rat ventricular myocytes, 2 to 4 hours of exposure to 10 micromol/L colchicine had no effect on shortening or [Ca(2+)](i) transient amplitude or on the amplitude of I(Ca,L) in perforated patch-clamped cells, under basal conditions and after stimulation with 1 micromol/L isoproterenol. However, in ruptured patch-clamped myocytes, basal I(Ca,L) was 2-fold higher after treatment with colchicine compared with vehicle and, in contrast to vehicle-treated cells, I(Ca,L) did not increase in response to isoproterenol. Cell width decreased during ruptured patch-clamp experiments in colchicine-treated but not vehicle-treated myocytes. We conclude that in cells with intact sarcolemma, colchicine does not modulate Ca(2+) signaling or the response to beta stimulation. However, the combination of microtubule disruption by colchicine and the ruptured patch configuration activates I(Ca,L) and attenuates the response to beta stimulation. We propose that these effects may be due to loss of free tubulin by intracellular dialysis or to increased sensitivity to mechanical stimulation as a result of microtubule disruption. These findings have important implications for cardiomyopathies associated with decreased free tubulin or a diminished microtubular network. The full text of this article is available at http://www.circresaha.org.

Amphotericin B↗
PubMed2003

Peroxisome proliferator-activated receptor-alpha deficiency does not alter insulin sensitivity in mice maintained on regular or high-fat diet: hyperinsulinemic-euglycemic clamp studies.

Chronic peroxisome proliferator-activated receptor (PPAR)-alpha activation improves glucose metabolism in rodent models of insulin resistance and diabetes; however, PPAR-alpha deficiency was also reported to protect against high-fat diet (HFD)-induced insulin resistance. The aim of this study was to clarify the role of PPAR-alpha in the development of insulin resistance using PPAR-alpha knockout (KO) mice and wild-type controls (WT). Both WT and PPAR-alpha KO mice on HFD gained significantly more weight relative to chow-fed groups and displayed an increase in insulin levels and a decrease in adiponectin levels. Hyperinsulinemic-euglycemic clamp performed in the nonfasting state demonstrated that HFD caused a marked reduction in whole body, muscle, and white and brown adipose tissue glucose uptake in both WT and PPAR-alpha KO mice relative to chow-fed groups. Suppression of endogenous glucose production during the clamp was markedly blunted in both WT and PPAR-alpha KO HFD-fed mice, indicating liver insulin resistance. The magnitude of HFD-induced changes in the clamp parameters of insulin sensitivity was comparable in PPAR-alpha KO and WT mice. In conclusion, these data show that PPAR-alpha deficiency does not alter insulin sensitivity in mice fed normal chow diet and does not protect against HFD-induced insulin resistance as measured by hyperinsulinemic-euglycemic clamp in nonfasted state.

Adiponectin↗
PubMed2003

Modified quantitative insulin sensitivity check index is better correlated to hyperinsulinemic glucose clamp than other fasting-based index of insulin sensitivity in different insulin-resistant states.

Fasting-based index estimates of insulin sensitivity were compared with euglycemic hyperinsulinemic clamp (IS clamp) measurements in 148 subjects: normal controls (n = 46), and obese (n = 12), polycystic ovary syndrome (n = 16), first-degree relatives of type 2 diabetic (n = 17), impaired glucose tolerance (n = 28), and type 2 diabetic (n = 29) patients. The fasting-based indexes tested included log homeostasis model assessment (HOMA), the quantitative insulin sensitivity check index (QUICKI), the revised QUICKI, and a new revised QUICKI using fasting plasma glycerol. In the population studied, at 40 mU/m(2).min (n = 30) revised QUICKI (r = 0.86; P < 0.0001) and QUICKI-glycerol (r = 0.87; P < 0.0001) gave higher correlations with the IS clamp than QUICKI and log HOMA (r = 0.78 and r = -0.78; P < 0.001). For subjects tested at 75 mU/m(2).min (n = 118), comparable correlations were found for all indexes (r > 0.80; P < 0.0001). When studied in subgroups, revised QUICKI and QUICKI-glycerol give significantly higher correlations with the IS clamp than other indexes for lean control subjects studied at 40mU/m(2).min and impaired glucose tolerance subjects. We confirmed, in a large patient population with a wide range of insulin sensitivities, that no single test is superior in all groups of patients. However, QUICKI and revised QUICKI are good indexes that offer correlations similar to or higher than values obtained with log HOMA. Such indexes are simple tools to estimate insulin sensitivity appropriate for epidemiological studies.

Adolescent↗
PubMed2006

QPatch: the past, present and future of automated patch clamp.

The QPatch 16 significantly increases throughput for gigaseal patch clamp experiments, making direct measurements in ion channel drug discovery and safety testing feasible. Released to the market in the Autumn of 2004 by Sophion Bioscience, the QPatch originated from work done at NeuroSearch (Denmark) in the early days of automated patch clamp. Today, the QPatch provides many unique features. For example, only the QPatch includes an automated cell preparation station making several hours of unattended operation possible. The 16-channel electrode array, called the QPlate, includes glass-coated microfluidic channels for less compound absorption and, hence, more accurate IC(50) values. The microfluidic pathways also allow for very small amounts of compound used for each experiment ( approximately 5 microl per addition). Only the QPatch has four independent pipetting heads for more efficient liquid handling (especially for ligand-gated ion channel experiments). Patch clamp recordings with the QPatch match the high quality of conventional patch clamp and in some cases the results are even better. For example, only the QPatch includes 100% series resistance compensation for the elimination of false positives due to voltage errors. Finally, the modular QPatch 16 was designed with more channels in mind. The upgrade pathway to 48-channels (the QPatch HT) will be discussed.

Animals↗
PubMed2004

HERG channel (dys)function revealed by dynamic action potential clamp technique.

The human ether-a-go-go-related gene (HERG) encodes the rapid component of the cardiac delayed rectifier potassium current (I(Kr)). Per-Arnt-Sim domain mutations of the HERG channel are linked to type 2 long-QT syndrome. We studied wild-type and/or type 2 long-QT syndrome-associated mutant (R56Q) HERG current (I(HERG)) in HEK-293 cells, at both 23 and 36 degrees C. Conventional voltage-clamp analysis revealed mutation-induced changes in channel kinetics. To assess functional implication(s) of the mutation, we introduce the dynamic action potential clamp technique. In this study, we effectively replace the native I(Kr) of a ventricular cell (either a human model cell or an isolated rabbit myocyte) with I(HERG) generated in a HEK-293 cell that is voltage-clamped by the free-running action potential of the ventricular cell. Action potential characteristics of the ventricular cells were effectively reproduced with wild-type I(HERG), whereas the R56Q mutation caused a frequency-dependent increase of the action potential duration in accordance with the clinical phenotype. The dynamic action potential clamp approach also revealed a frequency-dependent transient wild-type I(HERG) component, which is absent with R56Q channels. This novel electrophysiological technique allows rapid and unambiguous determination of the effects of an ion channel mutation on the ventricular action potential and can serve as a new tool for investigating cardiac channelopathies.

Action Potentials↗
PubMed1992

Effects of growth hormone releasing hormone on insulin action and insulin secretion in a hypopituitary patient evaluated by the clamp technique.

The effect of growth hormone releasing hormone (GHRH-44) therapy on insulin action and secretion was evaluated in a hypopituitary patient after one month and one year of treatment. Hepatic and peripheral insulin action was studied with the hyperinsulinemic-euglycemic clamp in combination with [6,6-2H2]glucose tracer infusion. First and second phase insulin secretion was assessed with the hyperglycemic clamp. Prior to GHRH-44 therapy the hypopituitary patient had higher insulin mediated glucose disposal rate and lower basal and stimulated insulin concentrations by more than two standard deviations from the mean of a control group. Following therapy there was no change in basal hepatic glucose production; however, there was evidence of diminished peripheral insulin action. This was manifested by decreased insulin mediated glucose disposal during the hyperinsulinemic-euglycemic clamp, and increased insulin secretion during the hyperglycemic clamp. We conclude that GHRH-44 therapy in this patient was associated with decreased peripheral insulin action which was compensated for by increased insulin secretion.

Child↗
PubMed1993

The inter-relationship between insulin and chromium in hyperinsulinaemic euglycaemic clamps in healthy volunteers.

Evidence in the literature suggests that the trace element chromium may have a role in glucose homeostasis through the regulation of insulin action. We have previously reported a significant reduction in plasma chromium levels in healthy individuals, following a 75 g oral glucose load, and after meals and glucose-dependent uptake of chromium in insulin-dependent tissues in vitro. However, in vivo it is unclear whether the changes in plasma chromium relate to changes in plasma glucose or insulin. The present study describes a series of euglycaemic hyperinsulinaemic clamps designed to attempt to define the initiator of changes in plasma chromium levels in ten healthy individuals. The data showed a significant (P < 0.01) reduction in fasting plasma chromium levels following glucose infusion and an initial bolus of insulin. Significant (P < 0.02) increases in post-clamp urinary chromium excretion were insufficient to explain the decrease in plasma levels. During the recovery phase of an extended two-phase clamp protocol we found plasma insulin levels decreased by 70% within 10 min, associated with an increase in plasma chromium levels of 30% and no significant change in plasma glucose level. These data indicate that alterations in plasma glucose are unlikely to be directly related to changes in plasma chromium, whilst supporting the hypothesis that plasma insulin may influence plasma levels of this trace element. In contrast, plasma zinc was unaffected throughout these clamp studies.

Adult↗
PubMed2006

Considerations in the design of hyperinsulinemic-euglycemic clamps in the conscious mouse.

Despite increased use of the hyperinsulinemic-euglycemic clamp to study insulin action in mice, the effects of experimental parameters on the results obtained have not been addressed. In our studies, we determined the influences of sampling sites, fasting duration, and insulin delivery on results obtained from clamps in conscious mice. Carotid artery and jugular vein catheters were implanted in C57BL/6J mice (n = 6-10/group) fed a normal diet for sampling and infusions. After a 5-day recovery period, mice underwent a 120-min clamp (2.5-mU . kg(-1) . min(-1) insulin infusion; approximately 120-130 mg/dl glucose) while receiving [3-(3)H]glucose to determine glucose appearance (endoR(a)) and disappearance (R(d)). Sampling large volumes (approximately 100 mul) from the cut tail resulted in elevated catecholamines and basal glucose compared with artery sampling. Catecholamines were not elevated when taking small samples ( approximately 5 mul) from the cut tail. Overnight (18-h) fasting resulted in greater loss of total body, lean, and fat masses and hepatic glycogen but resulted in enhanced insulin sensitivity compared with 5-h fasting. Compared with a 16-mU/kg insulin prime, a 300-mU/kg prime resulted in hepatic insulin resistance and slower acquisition of steady-state glucose infusion rates (GIR) after a 5-h fast. The steady-state GIR was expedited after the 300-mU/kg prime in 18-h-fasted mice. The GIR and R(d) rose with increasing insulin infusions (0.8, 2.5, 4, and 20 mU . kg(-1) . min(-1)), but endoR(a) was fully suppressed with doses higher than 0.8 mU . kg(-1) . min(-1). Thus, common variations in experimental factors yield different results and should be considered in designing and interpreting clamps.

Animals↗
PubMed1996

In praise of the hyperglycemic clamp. A method for assessment of beta-cell sensitivity and insulin resistance.

The most widely used methods for the assessment of beta-cell response and peripheral tissue sensitivity to insulin include the oral glucose tolerance test (OGTT), the frequently sampled intravenous glucose tolerance test, and the hyperinsulinemiceuglycemic clamp technique. During an OGTT, glucose levels increase after a variable lag period, then reach a peak and fall variably among individuals. The response even varies in the same subject upon repeat testing. A more reproducible glucose curve is achieved with an intravenous glucose tolerance test in which the plasma glucose levels rise rapidly to a very high level and fall exponentially. In neither of the two methods is a steady-state glucose level achieved. In the hyperinsulinemic-euglycemic clamp technique, a steady-state glucose level can be maintained at any level of hyperinsulinemia. However, an assessment of beta-cell sensitivity is not obtained. The less used hyperglycemic clamp technique can assess beta-cell sensitivity as well as peripheral tissue sensitivity. Moreover, a measure of glucose effectiveness or non-insulin-mediated glucose uptake can also be determined. With this technique the beta-cells of all subjects are stimulated with the same arterial glucose concentration, thus enabling assessment of beta-cell response to identical plasma glucose levels. Comparison of responses to stable hyperglycemic stimuli can be made in glucose-tolerant and -intolerant states with the addition of various substances, either alone or in combination. The use of the hyperglycemic clamp and several of its variant forms is reviewed as an alternative method for assessment of glucose homeostasis.

Adult↗
PubMed1998

Insulin secretion in normal glucose-tolerant relatives of type 2 diabetic subjects. Assessments using hyperglycemic glucose clamps and oral glucose tolerance tests.

OBJECTIVE: To assess insulin secretion in normal glucose-tolerant Caucasian first-degree relatives of type 2 diabetes subjects and in matched normal glucose-tolerant control subjects and to compare insulin secretion as assessed using a hyperglycemic glucose clamp with insulin secretion as assessed using an oral glucose tolerance test (OGTT). RESEARCH DESIGN AND METHODS: Twenty-one first-degree relatives of type 2 diabetic subjects and 21 control subjects without a family history of type 2 diabetes, who were matched for sex, age, BMI, waist-to-hip ratio, and aerobic capacity, underwent a hyperglycemic glucose clamp (10 mmol/l, 180 min). An OGTT (75 g glucose in 300 ml water) was also performed. RESULTS: First-phase insulin release (plasma insulin, 0-10 min) was not different (multiple analysis of variance [MANOVA]: F = 2.63, P = 0.11). Second-phase insulin release was lower (MANOVA: F = 4.18, P = 0.047). Separate analyses of variance showed decreased plasma insulin levels from 120 min onward (all P < 0.05), decreasing to geometric mean (95% CI) levels of 330 (270-402) and 462 (366-582) pmol/l at 180 min in relatives and control subjects, respectively. The insulin sensitivity index (ISI) as assessed using a hyperglycemic clamp was not different between the two groups. Mean +/- SE ISI during the 3rd hour was 27.5 +/- 2.2 and 30.5 +/- 3.0 micrograms.kg-1.min-1.pmol-1.l-1 in relatives and control subjects, respectively (P > 0.20). At 90 min after the OGTT, log plasma insulin levels correlated significantly with second-phase insulin release as assessed using the hyperglycemic glucose clamp. CONCLUSIONS: Normal glucose-tolerant first-degree relatives of type 2 diabetic subjects have a decreased second-phase insulin release, compared with matched control subjects. After an OGTT, 90-min values of log plasma insulin and 90-min values of the ratio of log plasma insulin to blood glucose may be good indicators of insulin secretory properties in normal glucose-tolerant family members of type 2 diabetic subjects.

Adult↗
PubMed2004

Comparison of the [13C]glucose breath test to the hyperinsulinemic-euglycemic clamp when determining insulin resistance.

OBJECTIVE: With increasing emphasis on the recognition of the metabolic syndrome and early type 2 diabetes, a clinically useful measure of insulin resistance is desirable. The purpose of this study was to evaluate whether an index of glucose metabolism, as measured by (13)CO(2) generation from ingested [(13)C]glucose, would correlate with indexes from the hyperinsulinemic-euglycemic clamp. RESEARCH DESIGN AND METHODS: A total of 26 subjects with varying degrees of insulin sensitivity underwent both the [(13)C]glucose breath test and the hyperinsulinemic-euglycemic clamp. Results from the [(13)C]glucose breath test were compared with measures of insulin sensitivity from the glucose clamp as well as with other commonly used indexes of insulin sensitivity. RESULTS: There was a strong correlation between the [(13)C]glucose breath test result and the glucose disposal rate (r = 0.69, P < 0.0001) and insulin sensitivity index (r = 0.69, P < 0.0001) from the insulin clamp. The magnitude of these correlations compared favorably with QUICKI and were superior to the homeostasis model assessment. CONCLUSIONS: The [(13)C]glucose breath test may provide a useful noninvasive assessment of insulin sensitivity.

Adult↗
PubMed1999

Comparison of step and ramp voltage clamp on background currents in guinea-pig ventricular cells.

Isolated cardiac ventricular myocytes from guinea-pig were used to investigate the effect of voltage clamp protocols on background Na+ current (ib.Na) and inward rectifier current (i K1). Using long (4 s) clamp pulses and very long step clamps, the i-V relations showed that removal of Na+ reduces the amplitude and shifts the voltage dependence of i K1 (Spindler et al. 1998). Ramp clamps, however, gave more complicated results, with slower ramps more often giving the same results as steps and pulses. Both i K1 itself and, during faster ramps, other currents show hysteresis, so masking the steady-state changes. Using pulses, TTX had no effect on steady-state current. Small differences occurred in the ramps, but even at fast ramp speeds the effects are very much smaller than in Purkinje tissue. Only part of ib,Na is TTX sensitive and the effect does not occur in all cells.

Animals↗
PubMed2002

[Application of rat tail collagen in patch clamp experiment with vestibular hair cells].

OBJECTIVE: To study the feasibility of application of rat-tail collagen in patch clamp research in vestibular hair cells. METHODS: The effect of self-made rat-tail collagen on promoting adhesion of vestibular hair cells in whole cell patch clamp experiment was observed. RESULTS: A seal was hard to be formed when the vestibular hair cells suspended among the external solution without rat-tail collagen. However, when the vestibular hair cells were firmly adhesive to the bottom of the recording chamber with rat-tail collagen, a seal can be formed easily, which fitted to the long-term observation and recording. The effect of rat-tail collagen on adhesive to vestibular hair cells is obvious. CONCLUSION: Rat-tail collagen could facilitate the vestibular hair cells to adhesive with the bottom of the recording chamber, which is helpful for long-term patch clamp research, and the collagen is considered as an optimal adhesive reagent to vestibular hair cells for patch clamp research.

Animals↗