Methylsulfonylmethane (MSM), an organosulfur compound, is effective against obesity-induced metabolic disorders in mice.
Methylsulfonylmethane (MSM), an organosulfur compound, has been used as a dietary supplement that can improve various metabolic diseases. However, the effect of MSM on obesity-linked metabolic disorders remains unclear. The goal of the current study is to determine whether MSM has beneficial effects on glucose and lipid homeostasis in obesity-associated pathophysiologic states. High-fat diet-induced obese (DIO) and genetically obese diabetic db/db mice treated with MSM (1%-5% v/v, by drinking water) were studied. Metabolic parameters involved in glucose and lipid metabolism were determined. Treatment of DIO mice with MSM leads to a significant decrease in blood glucose levels. DIO mice treated with MSM are hypersensitive to insulin, as evidenced by decreased serum insulin and an increase in the area above the curve during an ITT. Concurrently, MSM reduces hepatic triglyceride and cholesterol contents in DIO mice. These effects are accompanied by reductions in gene expression of key molecules involved in lipogenesis and inflammation. FACS analysis reveals that MSM markedly increases the frequency of B cells and decreases the frequency of myeloid cells in peripheral blood and in bone marrow. Moreover, overnutrition-induced changes of femur microarchitecture are restored by MSM. In db/db mice, a marked impairment in glucose and lipid metabolic profiles is notably ameliorated when MSM is supplemented. These data suggest that MSM has beneficial effects on multiple metabolic dysfunctions, including hyperglycemia, hyperinsulinemia, insulin resistance, and inflammation. Thus, MSM could be the therapeutic option for the treatment of obesity-related metabolic disorders such as type 2 diabetes and fatty liver diseases.
Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA; Centro de Estudos de Doenças Crónicas CEDOC, NOVA Medical School/Faculdade de Ciências Médicas, Universidade Nova de Lisboa, Lisbon, Portugal.
Inês
I
Sousa-Lima
Boston Children's Hospital and Harvard Medical School, Boston, MA, USA.
Shin-Young
SY
Park
Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA.
Michelle
M
Chung
Department of Oriental Pharmacy, Wonkwang University, Iksan, Jeonbuk, Republic of Korea.
Hyun Ju
HJ
Jung
Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA.
Min-Cheol
MC
Kang
Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA; Centro de Estudos de Doenças Crónicas CEDOC, NOVA Medical School/Faculdade de Ciências Médicas, Universidade Nova de Lisboa, Lisbon, Portugal.
Joana M
JM
Gaspar
Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA.
Ji A
JA
Seo
Centro de Estudos de Doenças Crónicas CEDOC, NOVA Medical School/Faculdade de Ciências Médicas, Universidade Nova de Lisboa, Lisbon, Portugal; APDP - Education and Research Center, Lisbon, Portugal.
M Paula
MP
Macedo
Department of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science and Technology, Seoul National University; Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Republic of Korea.
Kyong Soo
KS
Park
Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA.
Christos
C
Mantzoros
YBSH Inc. Seoul, Republic of Korea.
Seung-Hoon
SH
Lee
Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA; Department of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science and Technology, Seoul National University. Electronic address: ykim2@bidmc.harvard.edu.
Young-Bum
YB
Kim
D041721:3T3-L1 Cells; D000818:Animals; D019440:Anti-Obesity Agents / Q000627:therapeutic use*; D001402:B-Lymphocytes / Q000187:drug effects; D001786:Blood Glucose / Q000378:metabolism; D002784:Cholesterol / Q000378:metabolism; D059305:Diet, High-Fat; D004121:Dimethyl Sulfoxide / Q000627:therapeutic use*; D005269:Femur / Q000473:pathology; D015870:Gene Expression / Q000187:drug effects; D007333:Insulin Resistance; D050356:Lipid Metabolism / Q000187:drug effects; D008099:Liver / Q000378:metabolism; D008297:Male; D008659:Metabolic Diseases / Q000188:drug therapy* / Q000209:etiology*; D051379:Mice; D008810:Mice, Inbred C57BL; D008820:Mice, Obese; D022423:Myeloid Cells / Q000187:drug effects; D009765:Obesity / Q000150:complications* / Q000235:genetics / Q000473:pathology; D013450:Sulfones / Q000627:therapeutic use*; D014280:Triglycerides / Q000378:metabolism
D019440:Anti-Obesity Agents; D001786:Blood Glucose; D013450:Sulfones; D014280:Triglycerides; D002784:Cholesterol; C025910:dimethyl sulfone; D004121:Dimethyl Sulfoxide
Hepatic steatosis; Inflammation; Methylsulfonylmethane; Obesity; Type 2 diabetes