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Identification of Ganglioside GM3 Molecular Species in Human Serum Associated with Risk Factors of Metabolic Syndrome.

Veillon L, Go S, Matsuyama W, Suzuki A, Nagasaki M, Yatomi Y, Inokuchi J - PLoS ONE (2015)

Bottom Line: A total of 23 GM3 molecular species were measured, of these, eight were found to be significantly elevated in individuals with visceral fat accumulation and metabolic disease, defined as the presence of hyperglycemia and dyslipidemia.The hydroxylated GM3 species were, in order of decreasing abundance, d18:1-h24:0 ≈ d18:1-h24:1 > d18:1-h22:0 » d18:1-h20:0 > d18:1-h21:0 > d18:1-h18:1.Univariate and multiple linear regression analyses were conducted using a number of clinical health variables associated with obesity, type 2 diabetes, metabolic disease, atherosclerosis and hypertension.

View Article: PubMed Central - PubMed

Affiliation: Division of Glycopathology, Institute of Molecular Biomembrane and Glycobiology, Tohoku Pharmaceutical University, Sendai, Japan.

ABSTRACT
Serum GM3 molecular species were quantified in 125 Japanese residents using tandem mass spectrometry multiple reaction monitoring. Individuals were categorized by the presence or absence of metabolic disease risk factors including visceral fat accumulation, hyperglycemia and dyslipidemia. A total of 23 GM3 molecular species were measured, of these, eight were found to be significantly elevated in individuals with visceral fat accumulation and metabolic disease, defined as the presence of hyperglycemia and dyslipidemia. All of the GM3 molecular species were composed of the sphingoid base sphingosine (d18:1 (Δ4)) and, interestingly, six of the eight elevated GM3 molecular species contained a hydroxylated ceramide moiety. The hydroxylated GM3 species were, in order of decreasing abundance, d18:1-h24:0 ≈ d18:1-h24:1 > d18:1-h22:0 » d18:1-h20:0 > d18:1-h21:0 > d18:1-h18:1. Univariate and multiple linear regression analyses were conducted using a number of clinical health variables associated with obesity, type 2 diabetes, metabolic disease, atherosclerosis and hypertension. GM3(d18:1-h24:1) was identified as the best candidate for metabolic screening, proving to be significantly correlated with intima-media thickness, used for the detection of atherosclerotic disease in humans, and a number of metabolic disease risk factors including autotaxin, LDL-c and homeostatic model assessment insulin resistance (HOMA-IR).

No MeSH data available.


Related in: MedlinePlus

The sum of GM3 molecular species.Total GM3 (A) and total hydroxylated GM3 (B) detected in serum of patients with visceral fat accumulation (VFA) (n = 39), VFA with hyperglycemia (n = 15), VFA with dyslipidemia (n = 28) and VFA with both hyperglycemia and dyslipidemia (n = 17) compared with healthy lean control individuals (n = 26). Species were determined using LC-MS/MS MRM. Data are reported as means ± SD. * P ≤ 0.05, ** P ≤ 0.01, *** P ≤ 0.001, **** P ≤ 0.0001 metabolic risk factor groups vs. control; Mann-Whitney unpaired test.
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pone.0129645.g002: The sum of GM3 molecular species.Total GM3 (A) and total hydroxylated GM3 (B) detected in serum of patients with visceral fat accumulation (VFA) (n = 39), VFA with hyperglycemia (n = 15), VFA with dyslipidemia (n = 28) and VFA with both hyperglycemia and dyslipidemia (n = 17) compared with healthy lean control individuals (n = 26). Species were determined using LC-MS/MS MRM. Data are reported as means ± SD. * P ≤ 0.05, ** P ≤ 0.01, *** P ≤ 0.001, **** P ≤ 0.0001 metabolic risk factor groups vs. control; Mann-Whitney unpaired test.

Mentions: The four most abundant molecular species of GM3 detected in control subjects were GM3(d18:1–24:0), GM3(d18:1–16:0), GM3(d18:1–24:1) and GM3(d18:1–22:0) (Fig 1A). Eight GM3 molecular species were elevated in a statistically significant fashion (P < 0.05) in the individuals of VFA with metabolic disease, in order of decreasing abundance they were GM3(d18:1–20:0) (control, 0.610 ± 0.336 ng/μL vs metabolic disease, 0.956 ± 0.662 ng/μL), GM3(d18:1-h24:0) (control, 0.317 ± 0.204 ng/μL vs metabolic disease, 0.588 ± 0.357 ng/μL), GM3(d18:1-h24:1) (control, 0.316 ± 0.192 ng/μL vs metabolic disease, 0.546 ± 0.283 ng/μL), GM3(d18:1-h22:0) (control, 0.238 ± 0.145 ng/μL vs metabolic disease, 0.400 ± 0.252 ng/μL), GM3(d18:1-h20:0) (control, 0.041 ± 0.042 ng/μL vs metabolic disease, 0.101 ± 0.070 ng/μL), GM3(d18:1-h21:0) (control, 0.029 ± 0.031 ng/μL vs metabolic disease, 0.044 ± 0.035 ng/μL), GM3(d18:1-h18:1) (control, 0.005 ± 0.007 ng/μL vs metabolic disease, 0.013 ± 0.009 ng/μL) and GM3(d18:1–21:1) (control, 0.005 ± 0.007 ng/μL vs metabolic disease, 0.009 ± 0.008 ng/μL), (Fig 1A and 1B). Additionally, the individuals of VFA with hyperglycemia exhibited elevated levels of GM3(d18:1–22:0) (control, 1.339 ± 0.651 ng/μL vs VFA with hyperglycemia, 1.927 ± 0.906 ng/μL), GM3(d18:1-h24:0) (control, 0.317 ± 0.204 ng/μL vs VFA with hyperglycemia, 0.527 ± 0.311 ng/μL) and GM3(d18:1-h23:0) (control, 0.091 ± 0.093 ng/μL vs VFA with hyperglycemia, 0.155 ± 0.126 ng/μL) (Fig 1A and 1B). Total GM3 values were elevated in the VFA with hyperglycemia and VFA with metabolic disease groups with average values of 12.814 ± 4.509 ng/μL and 13.972 ± 5.237 ng/μL respectively, compared with the control group’s average value of 11.468 ± 3.771 ng/μL (Fig 2A). However, this difference was not deemed statistically significant due to variation within the groups. Total hydroxylated GM3 species were elevated, and this increase observed in the VFA with metabolic disease group was statistically significant (control, 1.508 ± 0.651 ng/μL vs metabolic disease, 2.316 ± 1.041 ng/μL) with a P value of 0.0073 (Fig 2B).


Identification of Ganglioside GM3 Molecular Species in Human Serum Associated with Risk Factors of Metabolic Syndrome.

Veillon L, Go S, Matsuyama W, Suzuki A, Nagasaki M, Yatomi Y, Inokuchi J - PLoS ONE (2015)

The sum of GM3 molecular species.Total GM3 (A) and total hydroxylated GM3 (B) detected in serum of patients with visceral fat accumulation (VFA) (n = 39), VFA with hyperglycemia (n = 15), VFA with dyslipidemia (n = 28) and VFA with both hyperglycemia and dyslipidemia (n = 17) compared with healthy lean control individuals (n = 26). Species were determined using LC-MS/MS MRM. Data are reported as means ± SD. * P ≤ 0.05, ** P ≤ 0.01, *** P ≤ 0.001, **** P ≤ 0.0001 metabolic risk factor groups vs. control; Mann-Whitney unpaired test.
© Copyright Policy
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4477979&req=5

pone.0129645.g002: The sum of GM3 molecular species.Total GM3 (A) and total hydroxylated GM3 (B) detected in serum of patients with visceral fat accumulation (VFA) (n = 39), VFA with hyperglycemia (n = 15), VFA with dyslipidemia (n = 28) and VFA with both hyperglycemia and dyslipidemia (n = 17) compared with healthy lean control individuals (n = 26). Species were determined using LC-MS/MS MRM. Data are reported as means ± SD. * P ≤ 0.05, ** P ≤ 0.01, *** P ≤ 0.001, **** P ≤ 0.0001 metabolic risk factor groups vs. control; Mann-Whitney unpaired test.
Mentions: The four most abundant molecular species of GM3 detected in control subjects were GM3(d18:1–24:0), GM3(d18:1–16:0), GM3(d18:1–24:1) and GM3(d18:1–22:0) (Fig 1A). Eight GM3 molecular species were elevated in a statistically significant fashion (P < 0.05) in the individuals of VFA with metabolic disease, in order of decreasing abundance they were GM3(d18:1–20:0) (control, 0.610 ± 0.336 ng/μL vs metabolic disease, 0.956 ± 0.662 ng/μL), GM3(d18:1-h24:0) (control, 0.317 ± 0.204 ng/μL vs metabolic disease, 0.588 ± 0.357 ng/μL), GM3(d18:1-h24:1) (control, 0.316 ± 0.192 ng/μL vs metabolic disease, 0.546 ± 0.283 ng/μL), GM3(d18:1-h22:0) (control, 0.238 ± 0.145 ng/μL vs metabolic disease, 0.400 ± 0.252 ng/μL), GM3(d18:1-h20:0) (control, 0.041 ± 0.042 ng/μL vs metabolic disease, 0.101 ± 0.070 ng/μL), GM3(d18:1-h21:0) (control, 0.029 ± 0.031 ng/μL vs metabolic disease, 0.044 ± 0.035 ng/μL), GM3(d18:1-h18:1) (control, 0.005 ± 0.007 ng/μL vs metabolic disease, 0.013 ± 0.009 ng/μL) and GM3(d18:1–21:1) (control, 0.005 ± 0.007 ng/μL vs metabolic disease, 0.009 ± 0.008 ng/μL), (Fig 1A and 1B). Additionally, the individuals of VFA with hyperglycemia exhibited elevated levels of GM3(d18:1–22:0) (control, 1.339 ± 0.651 ng/μL vs VFA with hyperglycemia, 1.927 ± 0.906 ng/μL), GM3(d18:1-h24:0) (control, 0.317 ± 0.204 ng/μL vs VFA with hyperglycemia, 0.527 ± 0.311 ng/μL) and GM3(d18:1-h23:0) (control, 0.091 ± 0.093 ng/μL vs VFA with hyperglycemia, 0.155 ± 0.126 ng/μL) (Fig 1A and 1B). Total GM3 values were elevated in the VFA with hyperglycemia and VFA with metabolic disease groups with average values of 12.814 ± 4.509 ng/μL and 13.972 ± 5.237 ng/μL respectively, compared with the control group’s average value of 11.468 ± 3.771 ng/μL (Fig 2A). However, this difference was not deemed statistically significant due to variation within the groups. Total hydroxylated GM3 species were elevated, and this increase observed in the VFA with metabolic disease group was statistically significant (control, 1.508 ± 0.651 ng/μL vs metabolic disease, 2.316 ± 1.041 ng/μL) with a P value of 0.0073 (Fig 2B).

Bottom Line: A total of 23 GM3 molecular species were measured, of these, eight were found to be significantly elevated in individuals with visceral fat accumulation and metabolic disease, defined as the presence of hyperglycemia and dyslipidemia.The hydroxylated GM3 species were, in order of decreasing abundance, d18:1-h24:0 ≈ d18:1-h24:1 > d18:1-h22:0 » d18:1-h20:0 > d18:1-h21:0 > d18:1-h18:1.Univariate and multiple linear regression analyses were conducted using a number of clinical health variables associated with obesity, type 2 diabetes, metabolic disease, atherosclerosis and hypertension.

View Article: PubMed Central - PubMed

Affiliation: Division of Glycopathology, Institute of Molecular Biomembrane and Glycobiology, Tohoku Pharmaceutical University, Sendai, Japan.

ABSTRACT
Serum GM3 molecular species were quantified in 125 Japanese residents using tandem mass spectrometry multiple reaction monitoring. Individuals were categorized by the presence or absence of metabolic disease risk factors including visceral fat accumulation, hyperglycemia and dyslipidemia. A total of 23 GM3 molecular species were measured, of these, eight were found to be significantly elevated in individuals with visceral fat accumulation and metabolic disease, defined as the presence of hyperglycemia and dyslipidemia. All of the GM3 molecular species were composed of the sphingoid base sphingosine (d18:1 (Δ4)) and, interestingly, six of the eight elevated GM3 molecular species contained a hydroxylated ceramide moiety. The hydroxylated GM3 species were, in order of decreasing abundance, d18:1-h24:0 ≈ d18:1-h24:1 > d18:1-h22:0 » d18:1-h20:0 > d18:1-h21:0 > d18:1-h18:1. Univariate and multiple linear regression analyses were conducted using a number of clinical health variables associated with obesity, type 2 diabetes, metabolic disease, atherosclerosis and hypertension. GM3(d18:1-h24:1) was identified as the best candidate for metabolic screening, proving to be significantly correlated with intima-media thickness, used for the detection of atherosclerotic disease in humans, and a number of metabolic disease risk factors including autotaxin, LDL-c and homeostatic model assessment insulin resistance (HOMA-IR).

No MeSH data available.


Related in: MedlinePlus