Ignet

Gene Information

Gene symbol: SAT1

Gene name: spermidine/spermine N1-acetyltransferase 1

HGNC ID: 10540

Synonyms: SSAT

Related Genes

#	Gene Symbol	Number of hits
1	ADIPOQ	1 hits
2	AGT	1 hits
3	AMD1	1 hits
4	AQP7	1 hits
5	CCL2	1 hits
6	CFDP1	1 hits
7	CNBP	1 hits
8	CRP	1 hits
9	IL1B	1 hits
10	IL6	1 hits
11	IL8	1 hits
12	INS	1 hits
13	LEP	1 hits
14	LPIN1	1 hits
15	MCL1	1 hits
16	ODC1	1 hits
17	PLCG1	1 hits
18	PPARG	1 hits
19	RARRES2	1 hits
20	RBP4	1 hits
21	SAA	1 hits
22	SCD	1 hits
23	SDS	1 hits
24	SERPINE1	1 hits
25	SREBF1	1 hits
26	TNF	1 hits
27	WARS	1 hits

Related Sentences

#	PMID	Sentence
1	6807668	The enzyme activity responses of SDH and SAT to hormonal manipulation previously reported do not necessarily reflect the observed changes in pathway flux reported in the present study.
2	12660870	Thus, visceral cells transfer and release fatty acids more extensively, have increased glucocorticoid and reduced thiazolidinedione responses, produce more angiotensinogen, interleukin-6 and plasminogen activator inhibitor-1, and secrete less leptin and adiponectin than SAT.
3	12829631	Expression of peroxisome proliferator-activated receptor-gamma1 and peroxisome proliferator-activated receptor-gamma2 in visceral and subcutaneous adipose tissue of obese women.
4	12829631	Data regarding the expression of peroxisome proliferator-activated receptor (PPAR)-gamma(1) and PPAR-gamma(2) in human visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) are conflicting.
5	12829631	Quantification of the expression of PPAR-gamma(1) and PPAR-gamma(2) in samples of VAT and SAT was performed by real-time RT-PCR.
6	12829631	In both SAT and VAT, the level of expression of PPAR-gamma(2) were >20-fold that of PPAR-gamma(1) (P < 0.001 for both).
7	12829631	However, only PPAR-gamma(1) was differentially expressed, its levels in SAT being 216 +/- 34% those in VAT (P < 0.001).
8	12829631	In a stepwise, multivariate regression analysis, the levels of PPAR-gamma(1) in both SAT and VAT were the major determinants of waist circumference (R(2) = 21% for both; P < 0.01).
9	12829631	Finally, leptin but not PPARs appeared as the single parameter explaining the largest part of the variability of BMI in our cohort of patients (R(2) = 22%, P < 0.001).
10	12829631	These results are consistent with the putative roles of PPAR-gamma(1) and PPAR-gamma(2) in carbohydrate metabolism and energy homeostasis, respectively.
11	17125596	Mice with targeted disruption of spermidine/spermine N1-acetyltransferase gene maintain nearly normal tissue polyamine homeostasis but show signs of insulin resistance upon aging.
12	17125596	Further characterization of SSAT knockout mice revealed insulin resistance at old age which supported the role of polyamine catabolism in glucose metabolism detected earlier with our SSAT overexpressing mice displaying enhanced basal metabolic rate, high insulin sensitivity and improved glucose tolerance.
13	17125596	Mice with targeted disruption of spermidine/spermine N1-acetyltransferase gene maintain nearly normal tissue polyamine homeostasis but show signs of insulin resistance upon aging.
14	17125596	Further characterization of SSAT knockout mice revealed insulin resistance at old age which supported the role of polyamine catabolism in glucose metabolism detected earlier with our SSAT overexpressing mice displaying enhanced basal metabolic rate, high insulin sensitivity and improved glucose tolerance.
15	17327444	Increases in adiponectin predict improved liver, but not peripheral, insulin sensitivity in severely obese women during weight loss.
16	17327444	Plasma concentrations of leptin decreased and adiponectin increased significantly by 1 month, and decreases in interleukin-6, C-reactive protein (CRP), and tumor necrosis factor-alpha were observed at 6 months of weight loss.
17	17327444	Longitudinal decreases in CRP (r = -0.53, P < 0.05) were associated with increases in S(i), and decreases in HOMA-IR were related to increases in adiponectin (r = -0.37, P < 0.05).
18	17327444	Decreases in VAT were more strongly related to increases in adiponectin and decreases in CRP than were changes in general adiposity or SAT.
19	17327444	Thus, in severely obese women, specific loss of VAT leads to acute improvements in hepatic insulin sensitivity mediated by increases in adiponectin and in peripheral insulin sensitivity mediated by decreases in CRP.
20	17578890	SAT probe effluents were analyzed for IL-1beta, IL-6, CXCL8 (IL-8), and TNF-alpha.
21	17578890	Local administration of insulin exerted a stimulatory effect on the inflammatory response of IL-6.
22	18650840	However, SAT adiponectin mRNA levels were similar in hypertensive and non-hypertensive patients (15.3+/-4.2 vs 15.3+/-5.0 a.u., P > 0.99).
23	19615702	The trafficking of glycerol from adipose and hepatic tissue is mainly mediated by 2 aquaporin channel proteins: AQP7 and AQP9, respectively.
24	19615702	Real-time quantification of AQP7 in SAT and VAT and hepatic AQP9 gene expression were performed.
25	19615702	Visceral adipose tissue AQP7 expression levels were significantly higher than SAT AQP7 (P = .009).
26	19615702	The correlation between SAT AQP7 and liver AQP9 was stronger in intolerant and type 2 diabetes mellitus subjects (r = 0.602, P = .011).
27	19615702	The trafficking of glycerol from adipose and hepatic tissue is mainly mediated by 2 aquaporin channel proteins: AQP7 and AQP9, respectively.
28	19615702	Real-time quantification of AQP7 in SAT and VAT and hepatic AQP9 gene expression were performed.
29	19615702	Visceral adipose tissue AQP7 expression levels were significantly higher than SAT AQP7 (P = .009).
30	19615702	The correlation between SAT AQP7 and liver AQP9 was stronger in intolerant and type 2 diabetes mellitus subjects (r = 0.602, P = .011).
31	19615702	The trafficking of glycerol from adipose and hepatic tissue is mainly mediated by 2 aquaporin channel proteins: AQP7 and AQP9, respectively.
32	19615702	Real-time quantification of AQP7 in SAT and VAT and hepatic AQP9 gene expression were performed.
33	19615702	Visceral adipose tissue AQP7 expression levels were significantly higher than SAT AQP7 (P = .009).
34	19615702	The correlation between SAT AQP7 and liver AQP9 was stronger in intolerant and type 2 diabetes mellitus subjects (r = 0.602, P = .011).
35	20019678	Subjects with T2D had higher VAT expression of molecules regulating inflammation (tumor necrosis factor-alpha (TNFalpha), macrophage inflammatory protein (MIP), interleukin-8 (IL-8)).
36	20019678	Fasting glucose related to VAT expression of TNFalpha, MIP, serum amyloid A (SAA), IL-1alpha, IL-1beta, IL-8, and IL-8 receptor.
37	20019678	Abdominal fat mass was related to VAT expression of MIP, SAA, cAMP response element-binding protein (CREBP), IL-1beta, and IL-8.
38	20019678	There were depot-specific differences in expression of serum T2D predictors: VAT expressed higher levels of complement C3; SAT expressed higher levels of retinol-binding protein-4 (RBP4), adiponectin, and leptin.
39	20095974	Animals that overexpress the genes encoding the inducible key enzymes of biosynthesis and catabolism, ODC and SSAT (spermidine/spermine N1-acetyltransferase) respectively, appear to possess the most pleiotropic phenotypes.
40	20095974	Disruption of the ODC or AdoMetDC [AdoMet (S-adenosylmethionine) decarboxylase] gene is not compatible with mouse embryogenesis, whereas mice with a disrupted SSAT gene are viable and show no harmful phenotypic changes, except insulin resistance at a late age.
41	20095974	Animals that overexpress the genes encoding the inducible key enzymes of biosynthesis and catabolism, ODC and SSAT (spermidine/spermine N1-acetyltransferase) respectively, appear to possess the most pleiotropic phenotypes.
42	20095974	Disruption of the ODC or AdoMetDC [AdoMet (S-adenosylmethionine) decarboxylase] gene is not compatible with mouse embryogenesis, whereas mice with a disrupted SSAT gene are viable and show no harmful phenotypic changes, except insulin resistance at a late age.
43	20530740	Our aim was to perform a cross-sectional analysis of VAT compared with subcutaneous (SAT) LPIN1 expression in a well-characterized obese cohort, its relation with the expression of genes involved in lipid metabolism, and the in vitro response to lipogenic and lipolytic stimuli.
44	21060977	Stearoyl-CoA desaturase-1 is associated with insulin resistance in morbidly obese subjects.
45	21060977	Animal studies have revealed the association between stearoyl-CoA desaturase 1 (SCD1) and obesity and insulin resistance.
46	21060977	We studied SCD1 in visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) from morbidly obese patients and their association with insulin resistance, sterol regulatory element binding protein-1 (SREBP-1) and ATPase p97, proteins involved in SCD1 synthesis and degradation.
47	21060977	Measurements were made of VAT and SAT SCD1, SREBP-1 and ATPase p97 mRNA expression and protein levels.
48	21060977	VAT and SAT SCD1 mRNA expression levels in the morbidly obese patients were significantly lower than in the controls (P = 0.006), whereas SCD1 protein levels were significantly higher (P < 0.001).
49	21060977	In the morbidly obese patients, the VAT SCD1 protein levels were decreased in patients with higher insulin resistance (P = 0.007).
50	21060977	However, SAT SCD1 protein levels were increased in morbidly obese patients with higher insulin resistance (P < 0.05).
51	21060977	Multiple linear regressions in the morbidly obese patients showed that the variable associated with the SCD1 protein levels in VAT was insulin resistance, and the variables associated with SCD1 protein levels in SAT were body mass index (BMI) and ATPase p97.
52	21060977	In conclusion, these data suggest that the regulation of SCD1 is altered in individuals with morbid obesity and that the SCD1 protein has a different regulation in the two adipose tissues, as well as being closely linked to the degree of insulin resistance.
53	21060977	Stearoyl-CoA desaturase-1 is associated with insulin resistance in morbidly obese subjects.
54	21060977	Animal studies have revealed the association between stearoyl-CoA desaturase 1 (SCD1) and obesity and insulin resistance.
55	21060977	We studied SCD1 in visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) from morbidly obese patients and their association with insulin resistance, sterol regulatory element binding protein-1 (SREBP-1) and ATPase p97, proteins involved in SCD1 synthesis and degradation.
56	21060977	Measurements were made of VAT and SAT SCD1, SREBP-1 and ATPase p97 mRNA expression and protein levels.
57	21060977	VAT and SAT SCD1 mRNA expression levels in the morbidly obese patients were significantly lower than in the controls (P = 0.006), whereas SCD1 protein levels were significantly higher (P < 0.001).
58	21060977	In the morbidly obese patients, the VAT SCD1 protein levels were decreased in patients with higher insulin resistance (P = 0.007).
59	21060977	However, SAT SCD1 protein levels were increased in morbidly obese patients with higher insulin resistance (P < 0.05).
60	21060977	Multiple linear regressions in the morbidly obese patients showed that the variable associated with the SCD1 protein levels in VAT was insulin resistance, and the variables associated with SCD1 protein levels in SAT were body mass index (BMI) and ATPase p97.
61	21060977	In conclusion, these data suggest that the regulation of SCD1 is altered in individuals with morbid obesity and that the SCD1 protein has a different regulation in the two adipose tissues, as well as being closely linked to the degree of insulin resistance.
62	21060977	Stearoyl-CoA desaturase-1 is associated with insulin resistance in morbidly obese subjects.
63	21060977	Animal studies have revealed the association between stearoyl-CoA desaturase 1 (SCD1) and obesity and insulin resistance.
64	21060977	We studied SCD1 in visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) from morbidly obese patients and their association with insulin resistance, sterol regulatory element binding protein-1 (SREBP-1) and ATPase p97, proteins involved in SCD1 synthesis and degradation.
65	21060977	Measurements were made of VAT and SAT SCD1, SREBP-1 and ATPase p97 mRNA expression and protein levels.
66	21060977	VAT and SAT SCD1 mRNA expression levels in the morbidly obese patients were significantly lower than in the controls (P = 0.006), whereas SCD1 protein levels were significantly higher (P < 0.001).
67	21060977	In the morbidly obese patients, the VAT SCD1 protein levels were decreased in patients with higher insulin resistance (P = 0.007).
68	21060977	However, SAT SCD1 protein levels were increased in morbidly obese patients with higher insulin resistance (P < 0.05).
69	21060977	Multiple linear regressions in the morbidly obese patients showed that the variable associated with the SCD1 protein levels in VAT was insulin resistance, and the variables associated with SCD1 protein levels in SAT were body mass index (BMI) and ATPase p97.
70	21060977	In conclusion, these data suggest that the regulation of SCD1 is altered in individuals with morbid obesity and that the SCD1 protein has a different regulation in the two adipose tissues, as well as being closely linked to the degree of insulin resistance.
71	21060977	Stearoyl-CoA desaturase-1 is associated with insulin resistance in morbidly obese subjects.
72	21060977	Animal studies have revealed the association between stearoyl-CoA desaturase 1 (SCD1) and obesity and insulin resistance.
73	21060977	We studied SCD1 in visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) from morbidly obese patients and their association with insulin resistance, sterol regulatory element binding protein-1 (SREBP-1) and ATPase p97, proteins involved in SCD1 synthesis and degradation.
74	21060977	Measurements were made of VAT and SAT SCD1, SREBP-1 and ATPase p97 mRNA expression and protein levels.
75	21060977	VAT and SAT SCD1 mRNA expression levels in the morbidly obese patients were significantly lower than in the controls (P = 0.006), whereas SCD1 protein levels were significantly higher (P < 0.001).
76	21060977	In the morbidly obese patients, the VAT SCD1 protein levels were decreased in patients with higher insulin resistance (P = 0.007).
77	21060977	However, SAT SCD1 protein levels were increased in morbidly obese patients with higher insulin resistance (P < 0.05).
78	21060977	Multiple linear regressions in the morbidly obese patients showed that the variable associated with the SCD1 protein levels in VAT was insulin resistance, and the variables associated with SCD1 protein levels in SAT were body mass index (BMI) and ATPase p97.
79	21060977	In conclusion, these data suggest that the regulation of SCD1 is altered in individuals with morbid obesity and that the SCD1 protein has a different regulation in the two adipose tissues, as well as being closely linked to the degree of insulin resistance.
80	21060977	Stearoyl-CoA desaturase-1 is associated with insulin resistance in morbidly obese subjects.
81	21060977	Animal studies have revealed the association between stearoyl-CoA desaturase 1 (SCD1) and obesity and insulin resistance.
82	21060977	We studied SCD1 in visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) from morbidly obese patients and their association with insulin resistance, sterol regulatory element binding protein-1 (SREBP-1) and ATPase p97, proteins involved in SCD1 synthesis and degradation.
83	21060977	Measurements were made of VAT and SAT SCD1, SREBP-1 and ATPase p97 mRNA expression and protein levels.
84	21060977	VAT and SAT SCD1 mRNA expression levels in the morbidly obese patients were significantly lower than in the controls (P = 0.006), whereas SCD1 protein levels were significantly higher (P < 0.001).
85	21060977	In the morbidly obese patients, the VAT SCD1 protein levels were decreased in patients with higher insulin resistance (P = 0.007).
86	21060977	However, SAT SCD1 protein levels were increased in morbidly obese patients with higher insulin resistance (P < 0.05).
87	21060977	Multiple linear regressions in the morbidly obese patients showed that the variable associated with the SCD1 protein levels in VAT was insulin resistance, and the variables associated with SCD1 protein levels in SAT were body mass index (BMI) and ATPase p97.
88	21060977	In conclusion, these data suggest that the regulation of SCD1 is altered in individuals with morbid obesity and that the SCD1 protein has a different regulation in the two adipose tissues, as well as being closely linked to the degree of insulin resistance.
89	23001483	In the present study, we aimed to test the hypotheses that (1) AQP7 is localized to the capillaries within human adipose tissue, (2) genetic predisposition to type-2 diabetes is associated with a low expression of AQP7 in abdominal subcutaneous adipose tissue (SAT) and (3) physical training increases AQP7 expression in SAT.
90	23001483	The relative expression of AQP7 protein in abdominal SAT was analysed before and after ending a 10-week exercise training programme in first-degree relatives to type-2 diabetic patients and control individuals.
91	23001483	We were unable to evidence a link between a low AQP7 abundance in SAT and genetic predisposition type-2 diabetes.
92	23001483	Instead we demonstrate that physical training influences the expression of AQP7 in SAT in a gender-specific manner.
93	23001483	In conclusion, the adipose tissue glycerol channel, AQP7, is regulated in response to physical training in a gender-dependent manner in SAT.
94	23001483	In the present study, we aimed to test the hypotheses that (1) AQP7 is localized to the capillaries within human adipose tissue, (2) genetic predisposition to type-2 diabetes is associated with a low expression of AQP7 in abdominal subcutaneous adipose tissue (SAT) and (3) physical training increases AQP7 expression in SAT.
95	23001483	The relative expression of AQP7 protein in abdominal SAT was analysed before and after ending a 10-week exercise training programme in first-degree relatives to type-2 diabetic patients and control individuals.
96	23001483	We were unable to evidence a link between a low AQP7 abundance in SAT and genetic predisposition type-2 diabetes.
97	23001483	Instead we demonstrate that physical training influences the expression of AQP7 in SAT in a gender-specific manner.
98	23001483	In conclusion, the adipose tissue glycerol channel, AQP7, is regulated in response to physical training in a gender-dependent manner in SAT.
99	23001483	In the present study, we aimed to test the hypotheses that (1) AQP7 is localized to the capillaries within human adipose tissue, (2) genetic predisposition to type-2 diabetes is associated with a low expression of AQP7 in abdominal subcutaneous adipose tissue (SAT) and (3) physical training increases AQP7 expression in SAT.
100	23001483	The relative expression of AQP7 protein in abdominal SAT was analysed before and after ending a 10-week exercise training programme in first-degree relatives to type-2 diabetic patients and control individuals.
101	23001483	We were unable to evidence a link between a low AQP7 abundance in SAT and genetic predisposition type-2 diabetes.
102	23001483	Instead we demonstrate that physical training influences the expression of AQP7 in SAT in a gender-specific manner.
103	23001483	In conclusion, the adipose tissue glycerol channel, AQP7, is regulated in response to physical training in a gender-dependent manner in SAT.
104	23001483	In the present study, we aimed to test the hypotheses that (1) AQP7 is localized to the capillaries within human adipose tissue, (2) genetic predisposition to type-2 diabetes is associated with a low expression of AQP7 in abdominal subcutaneous adipose tissue (SAT) and (3) physical training increases AQP7 expression in SAT.
105	23001483	The relative expression of AQP7 protein in abdominal SAT was analysed before and after ending a 10-week exercise training programme in first-degree relatives to type-2 diabetic patients and control individuals.
106	23001483	We were unable to evidence a link between a low AQP7 abundance in SAT and genetic predisposition type-2 diabetes.
107	23001483	Instead we demonstrate that physical training influences the expression of AQP7 in SAT in a gender-specific manner.
108	23001483	In conclusion, the adipose tissue glycerol channel, AQP7, is regulated in response to physical training in a gender-dependent manner in SAT.
109	23001483	In the present study, we aimed to test the hypotheses that (1) AQP7 is localized to the capillaries within human adipose tissue, (2) genetic predisposition to type-2 diabetes is associated with a low expression of AQP7 in abdominal subcutaneous adipose tissue (SAT) and (3) physical training increases AQP7 expression in SAT.
110	23001483	The relative expression of AQP7 protein in abdominal SAT was analysed before and after ending a 10-week exercise training programme in first-degree relatives to type-2 diabetic patients and control individuals.
111	23001483	We were unable to evidence a link between a low AQP7 abundance in SAT and genetic predisposition type-2 diabetes.
112	23001483	Instead we demonstrate that physical training influences the expression of AQP7 in SAT in a gender-specific manner.
113	23001483	In conclusion, the adipose tissue glycerol channel, AQP7, is regulated in response to physical training in a gender-dependent manner in SAT.
114	23296264	The aim of this study was to characterize adipocyte size and inflammatory profile in subcutaneous (SAT) and EAT among subjects with or without diabetes.
115	23296264	Biopsies were collected from SAT and EAT in 34 men undergoing elective cardiac surgery.
116	23296264	Weight, height, body mass index, waist circumference, as well as serum levels of glucose, insulin, lipids, adiponectin, and leptin were determined in all subjects.
117	23296264	Adiponectin, MCP-1, and CD68 mRNA levels present within cells from AT biopsies were determined by real-time polymerase chain reaction.
118	23296264	Regarding the experimental group as a whole, gene-expression levels within EAT were significantly lower for adiponectin and higher, albeit not significantly, for MCP-1, when compared with that of SAT.
119	23296264	Subjects with diabetes showed lower adiponectin gene-expression levels in both SAT and EAT when compared with subjects without diabetes.
120	23296264	By contrast, MCP-1 and CD68 gene-expression levels were higher in both tissue types of diabetic subjects.
121	23296264	Our data revealed a predominantly inflammatory profile in both SAT and EAT in subjects with diabetes in comparison with those without diabetes.
122	23296264	The aim of this study was to characterize adipocyte size and inflammatory profile in subcutaneous (SAT) and EAT among subjects with or without diabetes.
123	23296264	Biopsies were collected from SAT and EAT in 34 men undergoing elective cardiac surgery.
124	23296264	Weight, height, body mass index, waist circumference, as well as serum levels of glucose, insulin, lipids, adiponectin, and leptin were determined in all subjects.
125	23296264	Adiponectin, MCP-1, and CD68 mRNA levels present within cells from AT biopsies were determined by real-time polymerase chain reaction.
126	23296264	Regarding the experimental group as a whole, gene-expression levels within EAT were significantly lower for adiponectin and higher, albeit not significantly, for MCP-1, when compared with that of SAT.
127	23296264	Subjects with diabetes showed lower adiponectin gene-expression levels in both SAT and EAT when compared with subjects without diabetes.
128	23296264	By contrast, MCP-1 and CD68 gene-expression levels were higher in both tissue types of diabetic subjects.
129	23296264	Our data revealed a predominantly inflammatory profile in both SAT and EAT in subjects with diabetes in comparison with those without diabetes.
130	23296264	The aim of this study was to characterize adipocyte size and inflammatory profile in subcutaneous (SAT) and EAT among subjects with or without diabetes.
131	23296264	Biopsies were collected from SAT and EAT in 34 men undergoing elective cardiac surgery.
132	23296264	Weight, height, body mass index, waist circumference, as well as serum levels of glucose, insulin, lipids, adiponectin, and leptin were determined in all subjects.
133	23296264	Adiponectin, MCP-1, and CD68 mRNA levels present within cells from AT biopsies were determined by real-time polymerase chain reaction.
134	23296264	Regarding the experimental group as a whole, gene-expression levels within EAT were significantly lower for adiponectin and higher, albeit not significantly, for MCP-1, when compared with that of SAT.
135	23296264	Subjects with diabetes showed lower adiponectin gene-expression levels in both SAT and EAT when compared with subjects without diabetes.
136	23296264	By contrast, MCP-1 and CD68 gene-expression levels were higher in both tissue types of diabetic subjects.
137	23296264	Our data revealed a predominantly inflammatory profile in both SAT and EAT in subjects with diabetes in comparison with those without diabetes.
138	23296264	The aim of this study was to characterize adipocyte size and inflammatory profile in subcutaneous (SAT) and EAT among subjects with or without diabetes.
139	23296264	Biopsies were collected from SAT and EAT in 34 men undergoing elective cardiac surgery.
140	23296264	Weight, height, body mass index, waist circumference, as well as serum levels of glucose, insulin, lipids, adiponectin, and leptin were determined in all subjects.
141	23296264	Adiponectin, MCP-1, and CD68 mRNA levels present within cells from AT biopsies were determined by real-time polymerase chain reaction.
142	23296264	Regarding the experimental group as a whole, gene-expression levels within EAT were significantly lower for adiponectin and higher, albeit not significantly, for MCP-1, when compared with that of SAT.
143	23296264	Subjects with diabetes showed lower adiponectin gene-expression levels in both SAT and EAT when compared with subjects without diabetes.
144	23296264	By contrast, MCP-1 and CD68 gene-expression levels were higher in both tissue types of diabetic subjects.
145	23296264	Our data revealed a predominantly inflammatory profile in both SAT and EAT in subjects with diabetes in comparison with those without diabetes.
146	23653857	We have also shown that subjects with nascent MetS have increased the levels of SAT-secreted adipokines (IL-1, IL-6, IL-8, leptin, RBP-4, CRP, SAA, PAI-1, MCP-1, and chemerin) and plasma adipokines (IL-1, IL-6, leptin, RBP-4, CRP, SAA, and chemerin), as well as decreased levels of plasma adiponectin and both plasma and SAT omentin-1.