Effects of nutrition on the cell survival and gene expression of transplanted fat tissues in mice

Matsumoto, Fumiaki; Bujo, Hideaki; Kuramochi, Daichi; Saito, Kengo; Shibasaki, Manabu; Takahashi, Kazuo; Yoshimoto, Shinya; Ichinose, Masaharu; Saitō, Yasushi

doi:10.1016/s0006-291x(02)00711-8

Cited by 14 publications

(17 citation statements)

References 15 publications

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“…18,19) In diet-induced obesity, adipose tissue macrophages exhibit the phenotypic change from M2 to M1 during the course of obesity, thereby accelerating adipose tissue inflammation. 18,26,29) However, it was suggested that an obesity-induced switch in macrophage activation is coupled to the recruitment of an inflammatory subtype from the circulation, but not to the conversion of M2 to M1. 19) Although, in ddY-H mice, increased infiltration of macrophages was shown as described above, no change in gene expression of CD163 and MR, markers of M2 macrophage, 25) was observed.…”

Section: Discussionmentioning

confidence: 99%

“…15) CD11c, 25) toll-like receotor-4 (TLR4), 25) CD163, 25) mannose receptor (MR), 25) and β-actin. 26) Primers, which were purchased from Invitrogen (Carlsberg, CA, U.S.A.), were as follows: MCP-1, forward, 5′-CTT CTG GGC CTG CTG TTC A-3′, reverse, 5′-CCA GCC TAC TCA TTG GGA TCA -3′; F4/80, forward, 5′-CTT TGG CTA TGG GCT TCC AGT C-3′, reverse, 5′-GCA AGG AGG ACG AGT TTA TCG TG-3′, CD68, forward, 5′-CTT CCC ACA GGC AGC ACA G-3′, reverse, 5′-AAT GAT GAG AGG CAG CAA GAG G-3′; CD11c, forward, 5′-CTG GAT AGC CTT TCT TCT GCT G-3′, reverse,5′-GCA CAC TGT GTC CGA ACT C-3′; TLR4, forward, 5′-AGA AAT TCC TGC AGT GGG TCA -3′, reverse, 5′-TCT CTA CAG GTG TTG CAC ATG TCA -3′; CD163, forward, 5′-GGG TCA TTC AGA GGC ACA CTG -3′, reverse, 5′-CTG GCT GTC CTG TCA AGG CT-3′; MR, forward, 5′-CGG TGA ACC AAA TAA TTA CCA AAA T-3′, reverse, 5′-GTG GAG CAG GTG TGG GCT -3′; β-actin, forward, 5′-TGG AAT CCT GTG GCA TCC ATG AAA C-3′, reverse, 5′-TAA AAC GCA GCT CAG TAA CAG TCC G-3′. The amplification products obtained by RT-PCR were mixed with 10× Loading Buffer (TaKaRa, Tokyo, Japan) and were electorophoretically separated on 2% agarose gel.…”

Section: Methodsmentioning

confidence: 99%

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Infiltration of M1 Macrophages into Adipose Tissue of ddY-H Mice Preceding Spontaneous Appearances of Insulin Resistance

Maeda

Noge

Kagawa

2013

Biological & Pharmaceutical Bulletin

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We have isolated insulin resistant mice (ddY-H mice) which are spontaneously induced at 12-weeks of age even if fed with the standard chow pellets. Since accumulated evidences have suggested that an appearance of insulin resistance is associated with obesity and a state of inflammation in adipose tissue, the present study investigated an appearance of macrophages in adipose tissue of ddY-H mice. Although ddY-H mice were fed the standard chow pellets ad libitam, increases in body weight, adipose tissue mass, and fat cell size were observed. In adipose tissues of ddY-H mice, gene expression of monocyte chemoattractant protein-1 (MCP-1) elevated slightly at 5-weeks of age and was maintained at higher levels at 9-and 12-weeks of age, and MCP-1 content in adipose tissue increased 2-fold at 12-weeks of age. Also, increased gene expressions of CD68 and F4/80, markers of macrophage, in adipose tissue were observed at 9-weeks of age. In addition, F4/80 positive cells were histologically found in adipose tissue at 15-weeks of age but not at 7-weeks of age, suggesting an increased infiltration of macrophage into adipose tissue. In adipose tissue of ddY-H mice, gene expressions of CD11c and toll-like receptor 4 (TLR4), markers of proinflammatory macrophages (M1), markedly increased although those of CD163 and mannose receptor (MR), markers of anti-inflammatory macrophages (M2), did not change. These results suggest that proinflammatory (M1) macrophages infiltrate into enlarged adipose tissues of ddY-H mice, which is preceding spontaneous appearance of insulin resistance.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Infiltration of M1 Macrophages into Adipose Tissue of ddY-H Mice Preceding Spontaneous Appearances of Insulin Resistance

Maeda

Noge

Kagawa

2013

Biological & Pharmaceutical Bulletin

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“…The following primers were used: 5′-TGG AAT CCT GTG GCA TCC ATG AAA C-3′ and 5′-TAA AAC GCA GCT CAG TAA CAG TCC G-3′ for β-actin 20) ; 5′-GTA TGG TGT ATG AAG GCA ATG-3′ and 5′-CAG AGA ACG GAG GTG ACT-3′ for InsR 21) ; 5′-TGA TGT CAC CCA GTG GTA GTT GCT-3′ and 5′-TGG CAT GAG GAA GGG CAT GAG TAT-3′ for IRS-1 21) ; and 5′-AAA GTG GCC TAC AAC CCT TAC CCA-3′ and 5′-TCA TCG CTC TTG CAG CTA TTG GGA-3′ for IRS-2.…”

Section: Methodsmentioning

confidence: 99%

Age-Dependent Onset of Insulin Resistance in Insulin-Resistant Mice

Ide

Arisawa

Ogura

et al. 2015

Biological & Pharmaceutical Bulletin

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We have previously isolated spontaneous insulin-resistant mice (ddY-H) and non-insulin-resistant mice (ddY-L) from ddY mice. In the present study, age-dependent onset of insulin resistance in obese ddY-H mice was investigated by comparing with lean ddY-L mice. In ddY-H mice fed a standard diet, an increase in elevation of glucose-stimulated plasma insulin level, glucose intolerance in an intraperitoneal glucose tolerance test, and a reduction of hypoglycemic action of insulin were found at 9 weeks of age, but not at 6 weeks of age. When ddY-H mice were administered nateglinide, a greater elevation of plasma insulin level and a less decrease of serum glucose level were observed at 9 weeks of age. These changes developed progressively with age. These findings suggest that insulin resistance is induced at 9 weeks of age. The age-related change in insulin resistance was correlated with reductions in mRNA expression and protein content of the insulin receptor (InsR), and insulin receptor substrate (IRS)-1 and IRS-2 in the epididymal adipose tissue. On the other hand, in the liver, mRNA expression of InsR and IRS-1 did not change at any age, although that of the IRS-2 was reduced. Thus, in ddY-H mice, insulin resistance and glucose-stimulated hyper-secretion of insulin are induced at 9 weeks of age and are reciprocally affected, resulting in progression to a more severe state at an older age. Insulin resistance may be attributed, at least in part, to the decreases in the mRNA expressions and proteins of InsR, IRS-1 and IRS-2 in adipose tissue. Key words insulin resistance; age-related onset; insulin secretion; insulin receptor Type 2 diabetes mellitus is a complex disease characterized by hyperglycemia resulting from impaired pancreatic β-cell function and a decreased action of insulin on target tissues.

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“…Primers for CB1 were as follows: CB1 5′-GGTTCTGATCCTGGTGGTGTTGAT and 5′-CCGATGAGACAACAGACTTCT (GenBank accession: MM18374). Primers for β-actin were as described previously (27). Conditions for CB1 amplification were 35 cycles, for 1 minute each at 94°C, 55°C, and 72°C and conditions for β-actin were 35 cycles, for 1 minute each at 94°C, 60°C, and 72°C.…”

Section: Rna Isolation and Rt-pcrmentioning

confidence: 99%

The endogenous cannabinoid system affects energy balance via central orexigenic drive and peripheral lipogenesis

Cota¹,

Marsicano²,

Tschöp³

et al. 2003

J. Clin. Invest.

389

558

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A combination of central and peripheral mechanisms modulates food intake and energy consumption to maintain metabolism and body composition in mammals. Diseases characterized by impaired energy balance, such as obesity, rank among the most immediate health threats in industrialized countries, creating an urgent need to generate new pharmacologic treatment options (1, 2). The discovery of leptin has triggered intensified research efforts in the field of energy homeostasis, leading to a better understanding of a complex network of central and peripheral factors that influence both appetite and energy expenditure (3).The discovery of cannabinoid receptor type 1 (CB1) and cannabinoid receptro type 2 (CB2), provided a molecular basis for investigating the effects The cannabinoid receptor type 1 (CB1) and its endogenous ligands, the endocannabinoids, are involved in the regulation of food intake. Here we show that the lack of CB1 in mice with a disrupted CB1 gene causes hypophagia and leanness. As compared with WT (CB1 +/+ ) littermates, mice lacking CB1 (CB1 -/-) exhibited reduced spontaneous caloric intake and, as a consequence of reduced total fat mass, decreased body weight. In young CB1 -/-mice, the lean phenotype is predominantly caused by decreased caloric intake, whereas in adult CB1 -/-mice, metabolic factors appear to contribute to the lean phenotype. No significant differences between genotypes were detected regarding locomotor activity, body temperature, or energy expenditure. Hypothalamic CB1 mRNA was found to be coexpressed with neuropeptides known to modulate food intake, such as corticotropin-releasing hormone (CRH), cocaine-amphetamine-regulated transcript (CART), melanin-concentrating hormone (MCH), and prepro-orexin, indicating a possible role for endocannabinoid receptors within central networks governing appetite. CB1 -/-mice showed significantly increased CRH mRNA levels in the paraventricular nucleus and reduced CART mRNA levels in the dorsomedial and lateral hypothalamic areas. CB1 was also detected in epidydimal mouse adipocytes, and CB1-specific activation enhanced lipogenesis in primary adipocyte cultures. Our results indicate that the cannabinoid system is an essential endogenous regulator of energy homeostasis via central orexigenic as well as peripheral lipogenic mechanisms and might therefore represent a promising target to treat diseases characterized by impaired energy balance.

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Effects of nutrition on the cell survival and gene expression of transplanted fat tissues in mice

Cited by 14 publications

References 15 publications

Infiltration of M1 Macrophages into Adipose Tissue of ddY-H Mice Preceding Spontaneous Appearances of Insulin Resistance

Infiltration of M1 Macrophages into Adipose Tissue of ddY-H Mice Preceding Spontaneous Appearances of Insulin Resistance

Age-Dependent Onset of Insulin Resistance in Insulin-Resistant Mice

The endogenous cannabinoid system affects energy balance via central orexigenic drive and peripheral lipogenesis

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