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

Abstract

BackgroundThe 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.MethodsEighty 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.ResultsMSG-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.ConclusionDaily 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.

An excessive increase in glutamate contributes to glucose-toxicity in β-cells via activation of pancreatic NMDA receptors in rodent diabetes

“…These results suggested that brief exposure to glutamate stimulated insulin secretion from β-cells. However, Boonnate has reported that daily consumption of dietary glutamate decreased the pancreatic β-cell mass in adult rats34. The present data showed that chronic high-glucose treatment doubled the glutamate content in culture media of RINm5f cells, indicating that endogenous glutamate may be released from β-cells under chronic hyperglycemic conditions.…”

The incretin system ABCs in obesity and diabetes – novel therapeutic strategies for weight loss and beyond

“…In fact, monosodium glutamate (MSG), a substance used to produce an animal model of obesity , was shown to annul the effects of GLP‐1 by destroying the ARC after subcutaneous injection in rodents . More recently, rats treated with MSG (2 mg g −1 body weight in drinking water, daily) showed a reduced pancreatic β ‐cell mass, accompanied by hemorrhagic and fibrotic lesions, although glucose homeostasis remained unaffected; this suggests that in the presence or susceptibility to diabetes or sodium chloride, the pancreas might functionally manifest the dietary MSG negative effect .…”

Monosodium glutamate restricts the adipogenic potential of 3T3‐L1 preadipocytes through mitotic clonal expansion

“…In this vein, culminating data point out a significant association between dietary MSG and increased abdominal or retroperitoneal body fat content either in the presence or absence of total body weight gain compared with control high caloric chow-fed rats (Collison et al, 2010;Afifi and Abbas, 2011;Khalaf and Arafat, 2015). The coexistence of adipocyte hypertrophy and the reduced proliferative capacity of APCs (hyperplasia) in MSGobese animals is consistent with the abnormal expansion of fat tissue in obesity, wherein the pathologically relevant adipocyte hypertrophy gain dominance over the hyperplasia in adapting to chronic energy surplus (Takasaki, 1978;Terry et al, 1981;Fernstrom et al, 1996;Kondoh et al, 2005;Ortiz et al, 2006;Collison et al, 2009;Boonnate et al, 2015;Huang et al, 2017). Adipocyte hypertrophy and associated inflammation in adipose tissue is the hallmark of obesity pathogenesis in both human subjects and animal models (Hill and Peters, 1998;He et al, 2008;Shi et al, 2010;Insawang et al, 2012;Thu Hien et al, 2013).…”