(1)H NMR relaxation times (T(1) and T(2)) in parenchyma tissue of apple can identify three populations of water with different relaxation characteristics. By following the uptake of Mn(2+) ions in the tissue it is shown that the observed relaxation times originate from particular water compartments: the vacuole, the cytoplasm, and the cell wall/extracellular space.Proton exchange between these compartments is controlled by the plasmalemma and tonoplast membranes. During the Mn(2+) penetration experiment, conditions occur that cause the relaxation times of protons of cytoplasmic water to be much shorter than their residence time in the cytoplasm. Then the tonoplast permeability coefficient P(d) for water can be calculated from the vacuolar T(1) and T(2) values to be 2.44 10(-5) m.s(-1).

The rise in blood glucose after lunch is less if breakfast has been eaten. The metabolic basis of this second-meal phenomenon remains uncertain. We hypothesized that storage of ingested glucose as glycogen could be responsible during the post-meal suppression of plasma NEFAs (non-esterified fatty acids; 'free' fatty acids). In the present study we determined the metabolic basis of the second-meal phenomenon. Healthy subjects were studied on two separate days, with breakfast and without breakfast in a random order. We studied metabolic changes after a standardized test lunch labelled with 3 g of 13C-labelled (99%) glucose. Changes in post-prandial muscle glycogen storage were measured using 13C magnetic resonance spectroscopy. The rise in plasma glucose after lunch was significantly less if breakfast had been taken (0.9+/-0.3 compared with 3.2+/-0.3 mmol/l, with and without breakfast respectively; P<0.001), despite comparable insulin responses. Pre-lunch NEFAs were suppressed after breakfast (0.13+/-0.03 compared with 0.51+/-0.04 mmol/l) and levels correlated positively with the maximum glucose rise after lunch (r=0.62, P=0.001). The increase in muscle glycogen signal was greater 5 h after lunch on the breakfast day (103+/-21 compared with 48+/-12 units; P<0.007) and correlated negatively with plasma NEFA concentrations before lunch (r=-0.48, P<0.05). The second-meal effect is associated with priming of muscle glycogen synthesis consequent upon sustained suppression of plasma NEFA concentrations.

. Real-time assessment of postprandial fat storage in liver and skeletal muscle in health and type 2 diabetes.

assessment of muscle glycogen storage after mixed meals in normal and type 2 diabetic subjects. Am J Physiol Endocrinol Metab 284: E688-E694, 2003. First published December 3, 2002 10.1152/ajpendo.00471.2002To understand the day-to-day pathophysiology of impaired muscle glycogen storage in type 2 diabetes, glycogen concentrations were measured before and after the consumption of sequential mixed meals (breakfast: 190.5 g carbohydrate, 41.0 g fat, 28.8 g protein, 1,253 kcal; lunch: 203.3 g carbohydrate, 48.1 g fat, 44.0 g protein, 1,497.5 kcal) by use of natural abundance 13 C magnetic resonance spectroscopy. Subjects with diet-controlled type 2 diabetes (n ϭ 9) and ageand body mass index-matched nondiabetic controls (n ϭ 9) were studied. Mean fasting gastrocnemius glycogen concentration was significantly lower in the diabetic group (57.1 Ϯ 3.6 vs. 68.9 Ϯ 4.1 mmol/l; P Ͻ 0.05). After the first meal, mean glycogen concentration in the control group rose significantly from basal (97.1 Ϯ 7.0 mmol/l at 240 min; P ϭ 0.005). After the second meal, the high level of muscle glycogen concentration in the control group was maintained, with a further rise to 108.0 Ϯ 11.6 mmol/l by 480 min. In the diabetic group, the postprandial rise was markedly lower than that of the control group (65.9 Ϯ 5.2 mmol/l at 240 min, P Ͻ 0.005, and 70.8 Ϯ 6.7 mmol/l at 480 min, P ϭ 0.01) despite considerably greater serum insulin levels (752.0 Ϯ 109.0 vs. 372.3 Ϯ 78.2 pmol/l at 300 min, P ϭ 0.013). This was associated with a significantly greater postprandial hyperglycemia (10.8 Ϯ 1.3 vs. 5.3 Ϯ 0.2 mmol/l at 240 min, P Ͻ 0.005). Basal muscle glycogen concentration correlated inversely with fasting blood glucose (r ϭ Ϫ0.55, P Ͻ 0.02) and fasting serum insulin (r ϭ Ϫ0.57, P Ͻ 0.02). The increment in muscle glycogen correlated with initial increment in serum insulin only in the control group (r ϭ 0.87, P Ͻ 0.002). This study quantitates for the first time the subnormal basal muscle glycogen concentration and the inadequate glycogen storage after meals in type 2 diabetes. type 2 diabetes; magnetic resonance spectroscopy; insulin resistance MAINTENANCE OF GLUCOSE HOMEOSTASIS after meals depends on storage of glucose as glycogen in muscle and liver, suppression of hepatic glucose output, and increase in glucose oxidation. Previous work has quantitated the extent of glycogen storage in the liver and muscle of healthy young subjects and has demonstrated that, in both organs, the postprandial increase peaks around 5 h, declining thereafter (35, 36). In type 2 diabetes, glucose homeostasis fails, and marked postprandial hyperglycemia is typical. Because the normal stimulation of muscle glycogen storage is controlled principally by insulin, and because insulin action in muscle is decreased in type 2 diabetes, it may be hypothesized that this contributes to the postprandial hyperglycemia. The practical importance of this has been emphasized by data linking the extent of postprandial hyperglycemia with the vascular complications of diabetes (9, 12).Under c...

The intrinsic nonuniformities in the transmit radiofrequency field from standard quadrature volume resonators at high field are particularly problematic for localized MRS in areas such as the temporal lobe, where a low signal-to-noise ratio and poor metabolite quantification result from destructive B₁⁺ field interference, in addition to line broadening and signal loss from strong susceptibility gradients. MRS of the temporal lobe has been performed in a number of neurodegenerative diseases at clinical fields, but a relatively low signal-to-noise ratio has prevented the reliable quantification of, for example, glutamate and glutamine, which are thought to play a key role in disease progression. Using a recently developed high-dielectric-constant material placed around the head, localized MRS of the medial temporal lobe using the stimulated echo acquisition mode sequence was acquired at 7 T. The presence of the material increased the signal-to-noise ratio of MRS by a factor of two without significantly reducing the sensitivity in other areas of the brain, as shown by the measured B₁⁺ maps. An increase in the receive sensitivity B₁⁻ was also measured close to the pads. The spectral linewidth of the unsuppressed water peak within the voxel of interest was reduced slightly by the introduction of the dielectric pads (although not to a statistically significant degree), a result confirmed by using a pad composed of lipid. Using LCmodel for quantitative analysis of metabolite concentrations, the increase in signal-to-noise ratio and the slight decrease in spectral linewidth contributed to statistically significant reductions in the Cramer-Rao lower bounds (CRLBs), also allowing the levels of glutamate and glutamine to be quantified with CRLBs below 20%.