ABSTRACT
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 ß-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 ß-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.
Subject(s)
Diet , Insulin-Secreting Cells/cytology , Insulin-Secreting Cells/metabolism , Sodium Glutamate/administration & dosage , Animals , Blood Glucose , Body Weight , Glucose Tolerance Test , Insulin/metabolism , Insulin-Secreting Cells/drug effects , Islets of Langerhans/cytology , Islets of Langerhans/metabolism , Islets of Langerhans/pathology , Male , Organ Size/drug effects , Rats , Time FactorsABSTRACT
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.
Subject(s)
Sodium Glutamate/adverse effects , Urolithiasis/etiology , Urologic Diseases/etiology , Animals , Eating/physiology , Electrolytes/blood , Electrolytes/urine , Kidney/pathology , Kidney Calculi/blood , Kidney Calculi/etiology , Kidney Calculi/pathology , Kidney Calculi/urine , Kidney Function Tests/methods , Male , Rats , Rats, Wistar , Sodium/metabolism , Urolithiasis/blood , Urolithiasis/pathology , Urolithiasis/urine , Urologic Diseases/blood , Urologic Diseases/pathology , Urologic Diseases/urine , Water/metabolismABSTRACT
BACKGROUND: Epidemiology and animal models suggest that dietary monosodium glutamate (MSG) may contribute to the onset of obesity and the metabolic syndrome. METHODS: Families (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. RESULTS: The 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. CONCLUSION: Higher amounts of individual MSG consumption are associated with the risk of having the metabolic syndrome and being overweight independent of other major determinants.
