Long term effects of high fat and sucrose diets on obesity and lymphocyte proliferation in mice

Sato-Mito, Natsuko; Suzui, Masatoshi; Yoshino, Haruka; Kaburagi, Tomoko; Sato, Kazuto

doi:10.1007/s12603-009-0155-1

Cited by 11 publications

(13 citation statements)

References 33 publications

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“…B‐cell activation in the lymphoid organs is a critical point in antibody production, so the evaluation of their frequency can provide a good insight of how obesity may be affecting the general allergic response. In this context, the spleen is the main site for B cells to complete their maturation, nevertheless obesity itself can impact the splenic leukocyte function and proliferation, mainly B and T cells . Interestingly, our results demonstrate that OVA itself is not able to affect B‐cell populations in the spleen; however, when associated with obesity, the allergen affected not only their frequency, but also their activation status.…”

Section: Discussionmentioning

confidence: 65%

Obesity affects peripheral lymphoid organs immune response in murine asthma model

et al. 2019

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Summary Asthma and obesity present rising incidence, and their concomitance is a reason for concern, as obese individuals are usually resistant to conventional asthma treatments and have more exacerbation episodes. Obesity affects several features in the lungs during asthma onset, shifting the T helper type 2 (Th2)/eosinophilic response towards a Th17/neutrophilic profile. Moreover, those individuals can present reduced atopy and delayed cytokine production. However, the impact of obesity on follicular helper T (Tfh) cells and B cells that could potentially result in antibody production disturbances are still unclear. Therefore, we aimed to assess the peripheral response to ovalbumin (OVA) in a concomitant model of obesity and asthma. Pulmonary allergy was induced, in both lean and obese female BALB/c mice, through OVA sensitizations and challenges. Mediastinal lymph nodes (MLNs) and spleen were processed for immunophenotyping. Lung was used for standard allergy analysis. Obese‐allergic mice produced less anti‐OVA IgE and more IgG2a than lean‐allergic mice. Dendritic cells (CD11c+ MHCIIhigh) expressed less CD86 and more PDL1 in obese‐allergic mice compared with lean‐allergic mice, in the MLNs. Meanwhile, B cells (CD19+ CD40+) were more frequent and the amount of PDL1/PD1+ cells was diminished by obesity, with the opposite effects in the spleen. Tfh cells (CD3+ CD4+ CXCR5+ PD1+) expressing FoxP3 were more frequent in obese mice, associated with the predominance of Th (CD3+ CD4+) cells expressing interleukin‐4/GATA3 in the MLNs and interleukin‐17A/RORγT in the spleen. Those modifications to the main components of the germinal centers could be resulting in the increased IgG2a production, which – associated with the Th17/neutrophilic profile – contributes to asthma worsening and represents an important target for future treatment strategies.

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Section: Discussionmentioning

confidence: 65%

Obesity affects peripheral lymphoid organs immune response in murine asthma model

et al. 2019

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“…In addition to the accelerated loss of bone caused by HF treatment, the immune system was also compromised by obesity, as reflected by the significant reduction of B cells in HFc mice relative to RD mice. The decrease in both bone marrow and circulating B cells indicates an impairment of hematopoiesis, which may expose the host to a greater susceptibility to infection and a host of other diseases (11, 44). Restoration of the B‐cell population in the HFv mice to RD levels through LIV suggests that mechanical signals, whether direct or introduced using exercise, serve to protect the immune system and that recovery from the disruption caused by obesity does not inherently require a reduction in adiposity but rather reestablishing healthy fate selection of the HSC progenitors.…”

Section: Discussionmentioning

confidence: 99%

“…C onsequences of obesity include type II diabetes (1), osteoporosis (2–8), and immune system dysfunction (9–11). Considering the close interactions between the immune and skeletal systems (12), it is plausible that an intervention effective in preserving bone mass may also help protect the immune system, ultimately reducing the severe systemic complications inherent to diabetes and obesity.…”

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confidence: 99%

“…Given the dichotomous early differentiation pathway of the HSC, an increased commitment toward one of these two lineages would inevitably decrease commitment toward the other. Indeed, obesity‐related immune system dysfunction, as characterized by a reduction of immune cell proliferation and function (10, 11), may in some part be caused by a bias of HSC differentiation away from the lymphoid lineage and help explain the increase in osteoclasts via the myeloid lineage (2, 4), the result of which is an accelerated loss of trabecular bone (2, 6). In the study reported here, we examine the effect of diet‐induced obesity on the skeletal and immune systems.…”

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confidence: 99%

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Bone structure and B‐cell populations, crippled by obesity, are partially rescued by brief daily exposure to low‐magnitude mechanical signals

Chan¹,

Adler²,

Green³

et al. 2012

FASEB j.

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Deterioration of the immune and skeletal systems, each of which parallel obesity, reflects a fragile interrelationship between adiposity and osteoimmunology. Using a murine model of diet-induced obesity, this study investigated the ability of mechanical signals to protect the skeletal-immune systems at the tissue, cellular, and molecular level. A long-term (7 mo) high-fat diet increased total adiposity (+62%), accelerated age-related loss of trabecular bone (-61%), and markedly reduced B-cell number in the marrow (-52%) and blood (-36%) compared to mice fed a regular diet. In the final 4 mo of the protocol, the application of low-magnitude mechanical signals (0.2 g at 90 Hz, 15 min/d, 5 d/wk) restored both bone structure and B cells to those levels measured in control mice fed a regular diet. These phenotypic outcomes were achieved, in part, by reductions in osteoclastic activity and a biasing of hematopoietic stem cell differentiation toward the lymphoid B-cell lineage and away from a myeloid fate. These results emphasize that obesity undermines both the skeletal and immune systems, yet brief exposure to mechanical signals, perhaps as a surrogate to the salutary influence of exercise, diminishes the consequences of diabetes and obesity, restoring bone structure and normalizing B-cell populations by biasing of the fate of stem cells through mechanosensitive pathways.

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“…In addition, considerably impaired immune function was reported in dietinduced obese (DIO) mice. [7,8] All these indicate that further study should focus on the fact that the simultaneous onset of metabolic diseases and the accompanied immune disturbance is closely related to inflammation. In addition, we must advance from simply confirming improvement in metabolic phenotypes to additionally confirming inflammation and immune restoration when a therapeutic agent is evaluated for metabolic syndrome.…”

mentioning

confidence: 99%

Aloe QDM complex enhances specific cytotoxic T lymphocyte killing in vivo in metabolic disease mice

Lee

Kim

et al. 2017

Bioscience, Biotechnology, and Biochemistry

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We developed spontaneous diet-induced metabolic disease in mice by feeding them a high-fat diet for 23 weeks and administered Aloe QDM complex for 16 weeks to examine its restorative effect on immune disorders and metabolic syndrome. A series of immune functional assays indicated Aloe QDM complex enhanced lymphocyte proliferation and antigen-specific immunity as determined by the restored functions of cytotoxic T lymphocytes (CTL) and IgG production. The elevated serum TNF-α level was also regulated by Aloe QDM complex treatment, which suggested its complex therapeutic potential. As for metabolic phenotypes, oral administration of Aloe QDM complex significantly improved diabetic symptoms, including high fasting glucose levels and glucose tolerance, and distinctly alleviated lipid accumulation in adipose and hepatic tissue. The simultaneous restoration of Aloe QDM complex on metabolic syndrome and host immune dysfunction, especially on the specific CTL killing was first elucidated in our study.

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Long term effects of high fat and sucrose diets on obesity and lymphocyte proliferation in mice

Cited by 11 publications

References 33 publications

Obesity affects peripheral lymphoid organs immune response in murine asthma model

Obesity affects peripheral lymphoid organs immune response in murine asthma model

Bone structure and B‐cell populations, crippled by obesity, are partially rescued by brief daily exposure to low‐magnitude mechanical signals

Aloe QDM complex enhances specific cytotoxic T lymphocyte killing in vivo in metabolic disease mice

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