Vitoon Prasongwattana

Incidence of urolithiasis in northeast Thailand.

Background:

Monosodium glutamate (MSG) intake is associated with the prevalence of metabolic syndrome in a rural Thai population

BackgroundEpidemiology and animal models suggest that dietary monosodium glutamate (MSG) may contribute to the onset of obesity and the metabolic syndrome.MethodsFamilies (n = 324) from a rural area of Thailand were selected and provided MSG as the sole source for the use in meal preparation for 10 days. Three hundred forty-nine subjects aged 35–55 years completed the study and were evaluated for energy and nutrient intake, physical activity, and tobacco smoking. The prevalence of overweight and obesity (BMI ≥ 25 kg/m2), insulin resistance (HOMA-IR >3), and the metabolic syndrome (ATP III criteria) were evaluated according to the daily MSG intake.ResultsThe prevalence of the metabolic syndrome was significantly higher in the tertile with the highest MSG intake. Further, every 1 g increase in MSG intake significantly increased the risk of having the metabolic syndrome (odds ratio 1.14, 95% confidence interval-CI- 1.12 - 1.28) or being overweight (odds ratio 1.16, 95% CI 1.04 - 1.29), independent of the total energy intake and the level of physical activity.ConclusionHigher amounts of individual MSG consumption are associated with the risk of having the metabolic syndrome and being overweight independent of other major determinants.

Blood and urinary aggregator and inhibitor composition in controls and renal-stone patients from northeastern Thailand.

Renal-stone disease (RSD) is common in the rural communities of northeastern Thailand. We report the biochemical composition of blood and urine in 25 healthy city dwellers (G1), 12 healthy village dwellers (G2) and 25 village dwellers who had RSD (G3). They were male with a range of ages between 20 and 50 years and were free of renal failure, urinary infection, urinary obstruction and systemic illness. The results showed that hypocitraturia, hypokalemia and hypokaliuria were more common in the latter 2 groups. The 24-h urinary citrate excretion correlated significantly with urinary potassium in G3 cases (r = 0.704, p = 0.0002). After potassium chloride supplementation, serum and urinary potassium increased remarkably (p less than 0.003 and p = 0.002, respectively), whereas urinary citrate remained unchanged. Our results suggest that the predominant abnormality in our RSD patients were hypocitraturia and potassium deficiency and that these may be related.

Serial analyses of postmortem changes in human skeletal muscle : A case study of alterations in proteome profile, histology, electrolyte contents, water composition, and enzyme activity

Postmortem tissues are frequently used in forensic investigation, clinical studies, and biomedical research. It is well known that the shorter period from death to analyses provides the more accurate results. However, the longest postmortem interval that still provides the reliable data remains unclear. We performed serial analyses of postmortem changes in proteome profile, histology, electrolyte contents, water composition, and enzyme activity in human vastus lateralis muscle from a male cadaver (died from a motorcycle accident). This uninjured muscle was sectioned into several 1‐cm3 cubes and stored in individual closed tubes at 4 or 25°C for 0, 2, 4, 6, 12, 24 or 48 h prior to proteomic, histological, chemical and biochemical analyses. At 4°C, the 2‐DE proteome profile remained unchanged until 24 h, when some poorly focused protein spots and significant decrease in the total number of visualized spots were observed. These changes were detectable earlier (12 h) in the samples stored at 25°C. Profound vacuolization and autolysis started at 24 and 6 h for the samples stored at 4ºC and 25°C, respectively. K and Mg contents began to increase at 12 and 48 h, respectively, for both temperatures. However, the increase in Na and Ca contents began at 24 h in the samples stored at 4°C, but started earlier (12 h) in those stored at 25°C. Water content started to decline at 48 and 24 h in the samples stored at 4 and 25°C, respectively. Muscle lactate dehydrogenase activity began to be out of range at 12 h for both temperatures. These findings demonstrate that storing the samples at 4°C could delay some of the aforementioned changes, which occurred more rapidly at 25°C. Our results also suggest that muscle proteome profile, histology, electrolyte contents, water composition, and enzyme activity should be analyzed within the optimal postmortem intervals, which vary among individual analyses, to obtain the most reliable data.

Monosodium Glutamate (MSG) Consumption Is Associated with Urolithiasis and Urinary Tract Obstruction in Rats

Background The peritoneal injection of monosodium glutamate (MSG) can induce kidney injury in adult rats but the effects of long-term oral intake have not been determined. Methods We investigated the kidney histology and function in adult male Wistar rats that were fed ad libitum with a standard rat chow pellet and water with or without the addition of 2 mg/g body weight MSG/day in drinking water (n=10 per group). Both MSG-treated and control animals were sacrificed after 9 months when renal function parameters, blood and urine electrolytes, and tissue histopathology were determined. Results MSG-treated rats were more prone to kidney stone formation, as represented by the alkaline urine and significantly higher activity product of calcium phosphate. Accordingly, 3/10 MSG-treated rats developed kidney stones over 9 months versus none of the control animals. Further, 2/10 MSG-treated rats but none (0/10) of the controls manifested hydronephrosis. MSG-treated rats had significantly higher levels of serum creatinine and potassium including urine output volume, urinary excretion sodium and citrate compared to controls. In contrast, MSG-treated rats had significantly lower ammonium and magnesium urinary excretion. Conclusion Oral MSG consumption appears to cause alkaline urine and may increase the risks of kidney stones with hydronephrosis in rats. Similar effects in humans must be verified by dedicated studies.

Metabolic enzymes, antioxidants, and cytoskeletal proteins are significantly altered in vastus lateralis muscle of K-depleted cadaveric subjects.

Molecular mechanisms underlying myopathy caused by prolonged potassium (K) depletion remain poorly understood. In the present study, we examined proteome profile of vastus lateralis muscle obtained from cadaveric subjects who had K depletion (KD) (muscle K<80 micromol/g wet weight) compared to those who had no KD (NKD) (muscle K>or=80 micromol/g wet weight) (n=6 per group). Muscle proteins were extracted, resolved by 2-DE, and visualized with CBB-R250 stain. Spot matching and intensity analysis revealed significant changes in levels of 11 (6 increased and 5 decreased) protein spots in the KD group. Q-TOF MS and MS/MS analyses identified these altered proteins as metabolic enzymes (aldehyde dehydrogenase 1A1, uridine diphosphoglucose pyrophosphorylase, enolase 1, cytosolic malate dehydrogenase, and carbonic anhydrase III), antioxidants (peroxiredoxin-3 isoform b), cytoskeletal proteins (slow-twitch skeletal troponin I and myosin light chain 2), and others. These altered proteins are involved in many cellular functions, including bioenergetics, acid-base regulation, oxidative stress response, and muscle contractility. Validation was done by Western blot analysis, which confirmed the increased level of peroxiredoxin-3 and decreased level of troponin-I in the KD muscle. Linear regression analysis also revealed a significant negative correlation between peroxiredoxin-3 level and muscle K content (r=-0.887; p<0.001), as well as a significant positive correlation between troponin-I level and muscle K content (r=0.618; p<0.05). Our results implicate the important roles these altered proteins play in the development of KD-associated myopathy.

Monosodium Glutamate Dietary Consumption Decreases Pancreatic β-Cell Mass in Adult Wistar Rats

Background The amount of dietary monosodium glutamate (MSG) is increasing worldwide, in parallel with the epidemics of metabolic syndrome. Parenteral administration of MSG to rodents induces obesity, hyperglycemia, hyperlipidemia, insulin resistance, and type 2 diabetes. However, the impact of dietary MSG is still being debated. We investigated the morphological and functional effects of prolonged MSG consumption on rat glucose metabolism and on pancreatic islet histology. Methods Eighty adult male Wistar rats were randomly subdivided into 4 groups, and test rats in each group were supplemented with MSG for a different duration (1, 3, 6, or 9 months, n=20 for each group). All rats were fed ad libitum with a standard rat chow and water. Ten test rats in each group were provided MSG 2 mg/g body weight/day in drinking water and the 10 remaining rats in each group served as non-MSG treated controls. Oral glucose tolerance tests (OGTT) were performed and serum insulin measured at 9 months. Animals were sacrificed at 1, 3, 6, or 9 months to examine the histopathology of pancreatic islets. Results MSG-treated rats had significantly lower pancreatic β-cell mass at 1, 6 and 9 months of study. Islet hemorrhages increased with age in all groups and fibrosis was significantly more frequent in MSG-treated rats at 1 and 3 months. Serum insulin levels and glucose tolerance in MSG-treated and untreated rats were similar at all time points we investigated. Conclusion Daily MSG dietary consumption was associated with reduced pancreatic β-cell mass and enhanced hemorrhages and fibrosis, but did not affect glucose homeostasis. We speculate that high dietary MSG intake may exert a negative effect on the pancreas and such effect might become functionally significant in the presence or susceptibility to diabetes or NaCl; future experiments will take these crucial cofactors into account.

Proteomic Analysis of Kidney in Rats Chronically Exposed to Monosodium Glutamate

Background Chronic monosodium glutamate (MSG) intake causes kidney dysfunction and renal oxidative stress in the animal model. To gain insight into the renal changes induced by MSG, proteomic analysis of the kidneys was performed. Methods Six week old male Wistar rats were given drinking water with or without MSG (2 mg/g body weight, n = 10 per group) for 9 months. Kidneys were removed, frozen, and stored at –75°C. After protein extraction, 2-D gel electrophoresis was performed and renal proteome profiles were examined with Colloidal Coomassie Brilliant Blue staining. Statistically significant protein spots (ANOVA, p<0.05) with 1.2-fold difference were excised and analyzed by LC-MS. Proteomic data were confirmed by immunohistochemistry and Western blot analyses. Results The differential image analysis showed 157 changed spots, of which 71 spots were higher and 86 spots were lower in the MSG-treated group compared with those in the control group. Eight statistically significant and differentially expressed proteins were identified: glutathione S-transferase class-pi, heat shock cognate 71 kDa, phosphoserine phosphatase, phosphoglycerate kinase, cytosolic glycerol-3-phosphate dehydrogenase, 2-amino-3-carboxymuconate-6-semialdehyde decarboxylase, α-ketoglutarate dehydrogenase and succinyl-CoA ligase. Conclusion The identified proteins are mainly related to oxidative stress and metabolism. They provide a valuable clue to explore the mechanism of renal handling and toxicity on chronic MSG intake.

Response to Dr. Roger’s letter: further studies are necessary in order to conclude a causal association between the consumption of monosodium L-glutamate (MSG) and the prevalence of metabolic syndrome in the rural Thai population

See related article: http://www.nutritionandmetabolism.com/content/10/1/14

Mechanism of Hypercalciuria in Renal Stone Patients in Northeast Thailand

The present study reports the response of renal stone formers (SF) residing in the rural area around Khon Kaen City (KKC) in the northeast of Thailand to an oral calcium load according to Pak et al. (1).