Quantitation of absolute 2H enrichment of plasma glucose by 2H NMR analysis of its monoacetone derivative.

A simple (2)H NMR method for quantifying absolute (2)H-enrichments in all seven aliphatic positions of glucose following its derivatization to monoacetone glucose is presented. The method is based on the addition of a small quantity of (2)H-enriched formate to the NMR sample. When the method was applied to [2-(2)H]monoacetone glucose samples prepared from [2-(2)H]glucose standards of known enrichments in the range of 0.2-2.5%, enrichment estimates derived by the NMR method were in good agreement with the real enrichment values of the [2-(2)H]glucose precursors. The measurement was also applied to monoacetone glucose derived from human plasma glucose samples following administration of (2)H(2)O and attainment of isotopic steady state, where glucose H2 and body water enrichment are equivalent. In these studies, the absolute H2 enrichment of plasma glucose estimated by the formate method was in good agreement with the (2)H-enrichment of body water measured by an independent method.     

Sources of hepatic glycogen synthesis during an oral glucose tolerance test: Effect of transaldolase exchange on flux estimates

Sources of hepatic glycogen synthesis during an oral glucose tolerance test were evaluated in six healthy subjects by enrichment of a 75‐g glucose load with 6.67% [U‐¹³C]glucose and 3.33% [U‐²H₇]glucose and analysis of plasma glucose and hepatic uridine diphosphate–glucose enrichments (sampled as urinary menthol glucuronide) by ²H and ¹³C nuclear magnetic resonance. The direct pathway contribution, as estimated from the dilution of [U‐¹³C]glucose between plasma glucose and glucuronide, was unexpectedly low (36 ± 5%). With [U‐²H₇]glucose, direct pathway estimates based on the dilution of position 3 ²H‐enrichment between plasma glucose and glucuronide were significantly higher (51 ± 6%, P = 0.05). These differences reflect the exchange of the carbon 4, 5, and 6 moiety of fructose‐6‐phosphate and glyceraldehyde‐3‐phosphate catalyzed by transaldolase. As further evidence of this exchange, ²H‐enrichments in glucuronide positions 4 and 5 were inferior to those of position 3. From the difference in glucuronide positions 5 and 3 enrichments, the fraction of direct pathway carbons that experienced transaldolase exchange was estimated at 21 ± 4%. In conclusion, the direct pathway contributes only half of hepatic glycogen synthesis during an oral glucose tolerance test. Glucose tracers labeled in positions 4, 5, or 6 will give significant underestimates of direct pathway activity because of transaldolase exchange. Magn Reson Med, 2009. © 2009 Wiley‐Liss, Inc.     

Glucose production pathways by 2H and 13C NMR in patients with HIV-associated lipoatrophy.

Patients with HIV taking protease inhibitors were selected for the presence (five subjects) or absence (five subjects) of lipoatrophy. Following an overnight fast, subjects were given oral (2)H(2)O in divided doses (5 mL/kg body water), [U-(13)C(3)] propionate (10 mg/kg), and acetaminophen (1000 mg). Glucose (from plasma) or acetaminophen glucuronide (from urine) were converted to monoacetone glucose for (2)H NMR and (13)C NMR analysis. The fraction of plasma glucose derived from gluconeogenesis was not significantly different between groups. However, flux from glycerol into gluconeogenesis relative to glucose production was increased from 0.20 +/- 0.13 among subjects without lipoatrophy to 0.42 +/- 0.12 (P < 0.05) among subjects with lipoatrophy, and the TCA cycle contribution was reduced. Lipoatrophy was associated with an abnormal profile of glucose production as assessed by (13)C and (2)H NMR of plasma and urine.     

2H2O incorporation into hepatic acetyl‐CoA and de novo lipogenesis as measured by Krebs cycle‐mediated 2H‐enrichment of glutamate and glutamine

Deuterated water is widely used for measuring de novo lipogenesis on the basis of quantifying lipid ²H‐enrichment relative to that of body water. However, incorporation of ²H‐enrichment from body water into newly synthesized lipid molecules is incomplete therefore the true lipid precursor enrichment differs from that of body water. We describe a novel measurement of de novo lipogenesis that is based on a true precursor‐product analysis of hepatic acetyl‐CoA and triglyceride methyl enrichments from deuterated water. After deuterated water administration to seven in situ and seven perfused livers, acetyl‐CoA methyl enrichment was inferred from ²H nuclear magnetic resonance analysis of hepatic glutamate/glutamine (Glx) enrichment and triglyceride methyl enrichment was directly determined by ²H nuclear magnetic resonance of triglycerides. Acetyl‐CoA ²H‐enrichment was 71% ± 1% that of body water for in situ livers and 53% ± 2% of perfusate water for perfused livers. From the ratio of triglyceride‐methyl/acetyl‐CoA enrichments, fractional de novo lipogenesis rates of 0.97% ± 0.09%/2 hr and 7.92% ± 1.47%/48 hr were obtained for perfused and in situ liver triglycerides, respectively. Our method reveals that acetyl‐CoA enrichment is significantly less than body water both for in situ and perfused livers. Furthermore, the difference between acetyl‐CoA and body water enrichments is sensitive to the experimental setting. Magn Reson Med, 2011. © 2011 Wiley Periodicals, Inc.     

Acetaminophen glucuronide and plasma glucose report identical estimates of gluconeogenesis and glycogenolysis for healthy and prediabetic subjects using the deuterated water method

Plasma glucose ²H‐enrichment in positions 5 (²H5) and 2 (²H2) from deuterated water (²H₂O) provides a measure of the gluconeogenic contribution to endogenous glucose production. Urinary glucuronide analysis can circumvent blood sampling but it is not known if glucuronide and glucose enrichments are equal. Thirteen subjects with impaired fasting glucose/impaired glucose tolerance and 11 subjects with normal fasting glucose and normal glucose tolerance ingested ²H₂O to ～0.5% body water and acetaminophen. Glucose and glucuronide ²H5 and ²H2 were measured by ²H NMR spectroscopy of monoacetone glucose. For normal fasting glucose/normal glucose tolerance, ²H5 was 0.23 ± 0.02% and 0.25 ± 0.02% for glucose and glucuronide, respectively, whereas ²H2 was 0.47 ± 0.01% and 0.49 ± 0.02%, respectively. For impaired fasting glucose/impaired glucose tolerance, ²H5 was 0.22 ± 0.01% and 0.26 ± 0.02% for glucose and glucuronide, respectively, whereas ²H2 was 0.46 ± 0.01% and 0.49 ± 0.02%, respectively. The gluconeogenic contribution to endogenous glucose production measured from glucose and glucuronide were identical for both normal fasting glucose/normal glucose tolerance (48 ± 4 vs. 51 ± 3%) and impaired fasting glucose/impaired glucose tolerance (48 ± 2 vs. 53 ± 3%). Magn Reson Med 70:315–319, 2013. © 2012 Wiley Periodicals, Inc.     

Sources of hepatic glucose production by 2H2O ingestion and Bayesian analysis of 2H glucuronide enrichment

The contribution of gluconeogenesis to hepatic glucose production (GP) was quantified after ²H₂O ingestion by Bayesian analysis of the position 2 and 5 ²H‐NMR signals (H2 and H5) of monoacetone glucose (MAG) derived from urinary acetaminophen glucuronide. Six controls and 10 kidney transplant (KTx) patients with cyclosporine A (CsA) immunosuppressant therapy were studied. Seven KTx patients were lean and euglycemic (BMI = 24.3 ± 1.0 kg/m²; fasting glucose = 4.7 ± 0.1 mM) while three were obese and hyperglycemic (BMI = 30.5 ± 0.7 kg/m²; fasting glucose = 7.1 ± 0.5 mM). For the 16 spectra analyzed, the mean coefficient of variation for the gluconeogenesis contribution was 10% ± 5%. This uncertainty was associated with a mean signal‐to‐noise ratio (SNR) of 79:1 and 45:1 for the MAG H2 and H5 signals, respectively. For control subjects, gluconeogenesis contributed 54% ± 7% of GP as determined by the mean and standard deviation (SD) of individual Bayesian analyses. For the lean/normoglycemic KTx subjects, the gluconeogenic contribution to GP was 62% ± 7% (P = 0.06 vs. controls), while hyperglycemic/obese KTx patients had a gluconeogenic contribution of 68% ± 3% (P < 0.005 vs. controls). These data suggest that in KTx patients, an increased gluconeogenic contribution to GP is strongly associated with obesity and hyperglycemia. Magn Reson Med 60:517–523, 2008. © 2008 Wiley‐Liss, Inc.     

Hepatic UDP-glucose 13C isotopomers from [U-13C]glucose: a simple analysis by 13C NMR of urinary menthol glucuronide.

Menthol glucuronide was isolated from the urine of a healthy 70-kg female subject following ingestion of 400 mg of peppermint oil and 6 g of 99% [U-(13)C]glucose. Glucuronide (13)C-excess enrichment levels were 4-6% and thus provided high signal-to-noise ratios (SNRs) for confident assignment of (13)C-(13)C spin-coupled multiplet components within each (13)C resonance by (13)C NMR. The [U-(13)C]glucuronide isotopomer derived via direct pathway conversion of [U-(13)C]glucose to [U-(13)C]UDP-glucose was resolved from [1,2,3-(13)C(3)]- and [1,2-(13)C(2)]glucuronide isotopomers derived via Cori cycle or indirect pathway metabolism of [U-(13)C]glucose. In a second study, a group of four overnight-fasted patients (63 +/- 10 kg) with severe heart failure were given peppermint oil and infused with [U-(13)C]glucose for 4 hr (14 mg/kg prime, 0.12 mg/kg/min constant infusion) resulting in a steady-state plasma [U-(13)C]glucose enrichment of 4.6% +/- 0.6%. Menthol glucuronide was harvested and glucuronide (13)C-isotopomers were analyzed by (13)C NMR. [U-(13)C]glucuronide enrichment was 0.6% +/- 0.1%, and the sum of [1,2,3-(13)C(3)] and [1,2-(13)C(2)]glucuronide enrichments was 0.9% +/- 0.2%. From these data, flux of plasma glucose to hepatic UDPG was estimated to be 15% +/- 4% that of endogenous glucose production (EGP), and the Cori cycle accounted for at least 32% +/- 10% of GP.     

Metabolic loss of deuterium from isotopically labeled glucose

The isotopically substituted molecule (6-¹³C, 1, 6, 6-²H₃)glucose was evaluated to determine whether metabolic ²H loss would prevent its use in quantitating pentose phosphate pathway (PPP) activity. PPP activity causes the C1 of glucose to be lost as CO₂, while C6 can appear in lactate. ²H NMR analysis of the lactate produced from this glucose can distinguish (3-²H)-lactate (from C1 of glucose) from (3-¹³C, 3, 3-²H_Z)lactate (from C6 of glucose). ²H NMR spectroscopic analysis of medium containing (4-¹³C, 1,6,6^?2H₃) glucose after incubation with cultured rat 9L glioma cells suggested a 30.8 ± 2.1% PPP activity as compared with 6.0 ± 0.8% from separate, parallel incubations with (1-¹³C)glucose and (6-¹³C)glucose. Subsequent experiments with other isotopically labeled glucose molecules suggest that this discrepancy is due to selective loss of ²H from the C1 position of glucose, catalyzed by phosphoman-nose isomerase. Failure to consider ²H exchange from the C1 and C6 positions of glucose can lead to incorrect conclusions in metabolic studies utilizing this and other deuterated or tritiated glucose molecules.     

Quantifying tracer levels of (2)H(2)O enrichment from microliter amounts of plasma and urine by (2)H NMR.

A simple and sensitive (2)H NMR measurement of (2)H(2)O enrichment from a 10 microl volume of body fluid is presented. The method allows (2)H-enrichment levels of 0.1% or above to be rapidly determined from 10 microl of plasma or urine. The measurement is insensitive to the presence of plasma protein, allowing direct analysis of (2)H(2)O enrichment from native plasma samples. Magn Reson Med 45:156-158, 2001.     

Simple measurement of gluconeogenesis by direct 2H NMR analysis of menthol glucuronide enrichment from 2H2O.

The contribution of gluconeogenesis to fasting glucose production was determined by a simple measurement of urinary menthol glucuronide (MG) 2H enrichment from 2H2O. Following ingestion of 2H2O (0.5% body water) during an overnight fast and a pharmacological dose (400 mg) of a commercial peppermint oil preparation the next morning, 364 micromol MG was quantitatively recovered from a 2-h urine collection by ether extraction and a 125 micromol portion was directly analyzed by 2H NMR. The glucuronide 2H-signals were fully resolved and their relative intensities matched those of the monoacetone glucose derivative. The pharmacokinetics and yields of urinary MG after ingestion of 400 mg peppermint oil as either gelatin or enteric-coated capsules 1 h before breakfast were quantified in five healthy subjects. Gelatin capsules yielded 197 +/- 81 micromol of MG from the initial 2-h urine collection while enteric-coated capsules gave 238 +/- 84 micromol MG from the 2- to 4-h urine collection.     

Localized proton NMR observation of [3-13C]lactate in stroke after [1-13C]glucose infusion.

To assess whether elevated lactate in stable stroke is being actively produced from blood glucose localized 1H NMR stimulated echo spectra were obtained from a patient in the region of a 32-day-old cortical infarct before and 60-100 min after infusion of [1-13C]glucose. Prior to the infusion the spectrum from the region of the infarct contained an elevated resonance from C3 lactate and a greatly reduced resonance from N-acetyl groups relative to an unaffected contralateral region. After the infusion two additional resonances were observed at 62 and -64 Hz relative to the unlabeled resonance of C3 lactate which were assigned on the basis of chemical shift and relative intensity to [3-13C]lactate. The [3-13C]lactate fractional enrichment in the infarct region was measured to be 32% which is within error one-half the average [1-13C]plasma glucose enrichment during the postinfusion NMR measurement. The result suggests that the stroke lactate pool was completely derived from infused glucose.     

Plasma glucose metabolism during exercise in humans

Plasma glucose is an important energy source in exercising humans, supplying between 20 and 50% of the total oxidative energy production and between 25 and 100% of the total carbohydrate oxidised during submaximal exercise. Plasma glucose utilisation increases with the intensity of exercise, due to an increase in glucose utilisation by each active muscle fibre, an increase in the number of active muscle fibres, or both. Plasma glucose utilisation also increases with the duration of exercise, thereby partially compensating for the progressive decrease in muscle glycogen concentration. When compared at the same absolute exercise intensity (i.e. the same VO2), reliance on plasma glucose is also greater during exercise performed with a small muscle mass, i.e. with the arms or just 1 leg. This may be due to differences in the relative exercise intensity (i.e. the %VO2peak), or due to differences between the arms and legs in their fitness for aerobic activity. The rate of plasma glucose utilisation is decreased when plasma free fatty acid or muscle glycogen concentrations are very high, effects which are probably mediated by increases in muscle glucose-6-phosphate concentration. However, glucose utilisation is also reduced during exercise following a low carbohydrate diet, despite the fact that muscle glycogen is also often lower. When exercise is performed at the same absolute intensity before and after endurance training, plasma glucose utilisation is lower in the trained state. During exercise performed at the same relative intensity, however, glucose utilisation may be lower, the same, or actually higher in trained than in untrained subjects, because of the greater absolute VO2 and demand for substrate in trained subjects during exercise at a given relative exercise intensity. Although both hyperglycaemia and hypoglycaemia may occur during exercise, plasma glucose concentration usually remains relatively constant. Factors which increase or decrease the reliance of peripheral tissues on plasma glucose during exercise are therefore generally accompanied by quantitatively similar increases or decreases in glucose production. These changes in total glucose production are mediated by changes in both hepatic glycogenolysis and hepatic gluconeogenesis. Glycogenolysis dominates under most conditions, and is greatest early in exercise, during high intensity exercise, or when dietary carbohydrate intake is high. The rate of gluconeogenesis is increased when exercise is prolonged, preceded by a restricted carbohydrate intake, or performed with the arms. Both glycogenolysis and gluconeogenesis appear to be decreased by endurance exercise training. These effects are due to changes in both the hormonal milieu and in the availability of hepatic glycogen and gluconeogenic precursors.(ABSTRACT TRUNCATED AT 400 WORDS)     

Quantifying endogenous glucose production and contributing source fluxes from a single 2H NMR spectrum

Endogenous glucose production (EGP), gluconeogenic and glycogenolytic fluxes by analysis of a single ²H‐NMR spectrum is demonstrated with 6‐hr and 24‐hr fasted rats. Animals were administered [1‐²H, 1‐¹³C]glucose, a novel tracer of glucose turnover, and ²H₂O. Plasma glucose enrichment from both tracers was quantified by ²H‐NMR analysis of monoacetone glucose. The 6‐hr fasted group (n = 7) had EGP rates of 95.6 ± 13.3 μmol/kg/min, where 56.2 ± 7.9 μmol/kg/min were derived from PEP; 12.1 ± 2.1 μmol/kg/min from glycerol, and 32.1 ± 4.9 μmol/kg/min from glycogen. The 24‐hr fasted group (n = 7) had significantly lower EGP rates (52.8 ± 7.2 μmol/kg/min, P = 0.004 vs. 6 hr) mediated by a significantly reduced contribution from glycogen (4.7 ± 5.9 μmol/kg/min, P = 0.02 vs. 6 hr) while PEP and glycerol contributions were not significantly different (39.5 ± 3.9 and 8.5 ± 1.2 μmol/kg/min, respectively). These estimates agree with previous assays of EGP fluxes in fasted rats obtained by multinuclear NMR analyses of plasma glucose enrichment from ²H₂O and ¹³C‐glucose tracers. Magn Reson Med, 2009. © 2009 Wiley‐Liss, Inc.     

Noninvasive method to obtain input function for measuring tissue glucose utilization of thoracic and abdominal organs

We have developed a method for the noninvasive estimation of regional tissue glucose utilization in humans that employs positron emission tomography (PET) and 2-(18F)fluoro-2-deoxy-d-glucose (FDG). Unlike other methods, the input function used in this method is obtained from the corrected time-activity curve of the descending aorta, not the left ventricle, because the descending aorta is relatively free of spillover from other organs and extends from the upper thorax to the lower abdomen. With this method the time-activity curve of the descending aorta must be corrected for the partial volume effect and the difference in counts between plasma and whole blood. Using the noninvasively obtained input function, regional tissue glucose utilization was calculated by Patlak graphic analysis. k1k3/(k2 + k3) was in good agreement with k1k3/(k2 + k3) calculated from the plasma input function by arterial sampling (r = 0.9995). These results suggest that the input function and regional tissue glucose utilization (not only of myocardium but also of other thoracic and abdominal organs) can be determined noninvasively.     

Myocardial glucose uptake measured with fluorodeoxyglucose: a proposed method to account for variable lumped constants.

Quantitative assessment of myocardial glucose uptake by the glucose tracer analog 2-deoxy-2-[18F]fluoro-D-glucose (FDG) depends on a correction factor (lumped constant [LC]), which may vary. We propose that this variability is caused by different affinities of FDG and glucose for membrane transport and phosphorylation and can be predicted from the time course of FDG retention. We therefore measured the LC under steady-state metabolic conditions and compared the results with values predicted from the tracer retention alone. METHODS: We measured rates of myocardial glucose uptake by tracer ([2-3H]glucose) and tracer analog methods (FDG) in isolated working Sprague-Dawley rat hearts perfused with Krebs buffer and glucose, or glucose plus insulin or beta-hydroxybutyrate. In separate experiments, we established the theoretical upper and lower limits for the LC (Rt and Rp), which are determined by the relative rates of FDG and glucose membrane transport (Rt, 1.73 +/- 0.22) and the relative rates of FDG and glucose phosphorylation (Rp, 0.15 +/- 0.04). RESULTS: The LC was decreased in the presence of insulin or beta-hydroxybutyrate or both (from 1.14 +/- 0.3 to 0.58 +/- 0.16 [insulin], to 0.75 +/- 0.17 [beta-hydroxybutyrate] or to 0.53 +/- 0.17 [both], P < 0.05). The time-activity curves of FDG retention reflected these changes. Combining the upper and lower limits for the LC with the ratio between unidirectional and steady-state FDG uptake rates allowed the prediction of individual LCs, which agreed well with the actually measured values (r = 0.96, P < 0.001). CONCLUSION: The LC is not a constant but is a predictable quotient. As a result of the fixed relation between tracer and tracee for both membrane transport and phosphorylation, the quotient can be determined from the FDG time-activity curve and true rates of myocardial glucose uptake can be measured.     

Quantitation of erythrocyte pentose pathway flux with [2-13C]glucose and 1H NMR analysis of the lactate methyl signal.

A simple and sensitive NMR method for quantifying excess (13)C-enrichment in positions 2 and 3 of lactate by (1)H NMR spectroscopy of the lactate methyl signal is described. The measurement requires neither signal calibrations nor the addition of a standard and accounts for natural abundance (13)C-contributions. As a demonstration, the measurement was applied to approximately 3 micromol of lactate generated by erythrocyte preparations incubated with [2-(13)C]glucose to determine the fraction of glucose metabolized by the pentose phosphate pathway (PP). PP fluxes were estimated from the ratio of excess (13)C-enrichment in lactate carbon 3 relative to carbon 2 in accordance with established metabolic models. Under baseline conditions, PP flux accounted for 7 +/- 2% of glucose consumption while in the presence of methylene blue, a classical activator of PP activity, its contribution increased to 27 +/- 10% of total glucose consumption (P < 0.01).     

基于MCMC方法的生物气溶胶袭击施放源项参数反演

生物气溶胶施放源项参数反演是生物气溶胶袭击危害评估的反问题,对危害评估及应急响应具有重要指导意义.本文基于贝叶斯推理方法,利用生物传感器检测数据和正向大气扩散模型,构造似然函数,采用结合Metropolis-Hasting算法的马尔可夫链蒙特卡洛(Markov chain Monte Carlo,MCMC)抽样,对施放源位置、高度、施放剂量进行反演.统计分析表明,反演结果和初始源项参数设置吻合非常好,证明了方法的有效性.     

高血压患者胰岛素抵抗机制的研究

通过对36例原发性高血压（EH）并胰岛素抵抗（IR）者，18例继发性高血压（SH）者和24例正常血压（NT）者葡糖糖耐量试验前后血浆胰岛素和血糖水平的观察。作者发现：（1）与SH不同，在嗜铬细胞瘤，肾炎性和肾血管性高血压等SH患者中不存在IR；因此，IR可能是EH患者的发病机制之一。而不是其血压升高后的结果；（2）通过观察EH患者口服葡萄糖耐量试验前后血浆胰岛素和血糖水平的变化，可部份检测其是否存在IR；（3）通过观察EHIR患者血浆胰岛素对糖负荷反应性的降低程度可判断其IR的程度。     

力竭运动过程中大鼠纹状体葡萄糖/乳酸代谢的实时观察

目的:通过实时观察一次性力竭运动过程中大鼠纹状体葡萄糖和乳酸浓度的动态变化规律,揭示运动性中枢疲劳形成过程中脑能量代谢的特征。方法:8周龄雄性Wistar大鼠20只分为两组,纹状体葡萄糖、乳酸测定组(第1组)和外周血葡萄糖、乳酸测定组(第2组),每组10只。采用微透析-电化学联用的活体检测技术,实时监测大鼠(第1组)在一次性力竭运动过程中纹状体细胞外液中葡萄糖和乳酸的代谢变化,并从尾静脉采血动态监测大鼠(第2组)外周血液中葡萄糖和乳酸浓度的变化。结果:(1)与安静状态相比,运动初期大鼠纹状体胞外乳酸浓度显著升高(P<0.05),运动后期直至恢复期均显著降低(P<0.05,P<0.01);而胞外葡萄糖浓度在运动初期无明显变化,在运动后期开始下降,甚至在恢复期的90分钟内仍显著低于安静水平(P<0.05,P<0.01)。(2)大鼠外周血糖浓度随着运动时间的延长而显著降低,在运动力竭以及恢复期血糖水平均显著低于安静水平(P<0.05,P<0.01);大鼠血乳酸浓度在力竭运动过程中显著高于安静时水平(P<0.05),而在运动结束后即迅速恢复至安静时水平。结论:力竭运动过程中,持续的外周低血糖导致脑对于葡萄糖摄取不足,出现脑葡萄糖和乳酸浓度降低,中枢能量物质葡萄糖和乳酸代谢的显著降低可能是产生运动性中枢疲劳的一个重要的神经生物学机制。     

A lineshape fitting model for 1H NMR spectra of human blood plasma.

A lineshape fitting model was constructed for classifying the overlapping information in the 1H NMR spectrum of human blood plasma. A reliable assignment of the overlapping fatty acid (-CH2-)n and -CH3 resonances of the various lipoproteins (VLDL, very low density lipoprotein; LDL, low density lipoprotein; HDL high density lipoprotein) is introduced, and for the first time detailed characteristics (chemical shifts, half linewidths, and relative intensities) of the individual lipoprotein components were obtained directly from the whole plasma spectrum. This was achieved by combining the constructed lineshape fitting model and the proper 400 MHz proton NMR measurements from blood plasma of a healthy donor, from fractions of the different lipoproteins, and from plasma samples in which the lipoprotein fractions were separately added. The results suggest fair promise of future applications of the rapid and easy NMR analysis of lipoprotein distribution in various research and clinical situations.