Infliximab treatment prevents hyperglycemia and the intensification of hepatic gluconeogenesis in an animal model of high fat diet-induced liver glucose overproduction

Haida, Karissa Satomi; Bertachini, Gabriela; Tavoni, Thauany Martins; Guilhermetti, Márcio; Loures, Marco Rocha; Bazotte, Roberto Barbosa

doi:10.1590/s1516-89132012000300009

Cited by 5 publications

(4 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Similar results were also found by Gonzalez-Gay et al ( 339 ) in insulin resistant patients, with RA ( Table II ). In addition, Haida et al ( 340 ) demonstrated that infliximab treatment prevents hyperglycemia and liver gluconeogenesis, in high fat diet-fed mice. Moreover, infliximab seems to ameliorate TNF-α-induced IR, in 3T3-L1 adipocytes, in vitro , by improving the insulin signaling pathway, via inhibition of protein tyrosine phosphatase 1B ( 341 ).…”

Section: Therapeutic Interventions On Inflammatory Mediators For the ...mentioning

confidence: 99%

Molecular and pathophysiological relationship between obesity and chronic inflammation in the manifestation of metabolic dysfunctions and their inflammation‑mediating treatment options (Review)

Varra,

Varras,

Varra

et al. 2024

Mol Med Rep

View full text Add to dashboard Cite

Obesity reaches up to epidemic proportions globally and increases the risk for a wide spectrum of co-morbidities, including type-2 diabetes mellitus (T2DM), hypertension, dyslipidemia, cardiovascular diseases, non-alcoholic fatty liver disease, kidney diseases, respiratory disorders, sleep apnea, musculoskeletal disorders and osteoarthritis, subfertility, psychosocial problems and certain types of cancers. The underlying inflammatory mechanisms interconnecting obesity with metabolic dysfunction are not completely understood. Increased adiposity promotes pro-inflammatory polarization of macrophages toward the M1 phenotype, in adipose tissue (AT), with subsequent increased production of pro-inflammatory cytokines and adipokines, inducing therefore an overall, systemic, low-grade inflammation, which contributes to metabolic syndrome (MetS), insulin resistance (IR) and T2DM. Targeting inflammatory mediators could be alternative therapies to treat obesity, but their safety and efficacy remains to be studied further and confirmed in future clinical trials. The present review highlights the molecular and pathophysiological mechanisms by which the chronic low-grade inflammation in AT and the production of reactive oxygen species lead to MetS, IR and T2DM. In addition, focus is given on the role of anti-inflammatory agents, in the resolution of chronic inflammation, through the blockade of chemotactic factors, such as monocytes chemotractant protein-1, and/or the blockade of pro-inflammatory mediators, such as IL-1β, ΤΝF-α, visfatin, and plasminogen activator inhibitor-1, and/or the increased synthesis of adipokines, such as adiponectin and apelin, in obesity-associated metabolic dysfunction.

show abstract

Section: Therapeutic Interventions On Inflammatory Mediators For the ...mentioning

confidence: 99%

Molecular and pathophysiological relationship between obesity and chronic inflammation in the manifestation of metabolic dysfunctions and their inflammation‑mediating treatment options (Review)

Varra,

Varras,

Varra

et al. 2024

Mol Med Rep

View full text Add to dashboard Cite

show abstract

“…[1][2][3][4][5][6] Taking into account that the typical diet of Western countries is high in fat, 7,8 mice fed with HFD provide a model that more accurately represents the typical human diet compared with models where mice are fed with a balanced standard chow. [12][13][14] However, there are few studies regarding the effects of dietary enrichment with ɷ-3 polyunsaturated fatty acid [linseed oil (LO)] or ɷ-9 monosaturated fatty acid [macadamia oil (MO)] on the metabolic changes induced by HFD. 9,11 This HFD experimental model was also shown to be suitable to demonstrate the possibility to prevent or reverse the metabolic changes induced by an HFD.…”

Section: Introductionmentioning

confidence: 99%

“…9,11 This HFD experimental model was also shown to be suitable to demonstrate the possibility to prevent or reverse the metabolic changes induced by an HFD. [12][13][14] However, there are few studies regarding the effects of dietary enrichment with ɷ-3 polyunsaturated fatty acid [linseed oil (LO)] or ɷ-9 monosaturated fatty acid [macadamia oil (MO)] on the metabolic changes induced by HFD. 15,16 Moreover, to the best of our knowledge, the impact of LO and MO in the hyperglycaemic state and liver glucose overproduction induced by an HFD in mice has not previously been investigated.…”

Section: Introductionmentioning

confidence: 99%

Effect of linseed oil and macadamia oil on metabolic changes induced by high‐fat diet in mice

Barrena

Schiavon

Cararra

et al. 2013

Cell Biochemistry & Function

View full text Add to dashboard Cite

The effects of linseed oil (LO) and macadamia oil (MO) on the metabolic changes induced by a high-fat diet (HFD) rich in saturated fatty acid were investigated. For the purpose of this study, the vegetable oil present in the HFD, i.e. soybean oil (SO) was replaced with LO (HFD-LO) or MO (HFD-MO). For comparative purposes, a group was included, which received a normal fat diet (NFD). Male Swiss mice (6-week old) were used. After 14 days under the dietary conditions, the mice were fasted for 18 h, and experiments were then performed. The HFD-SO, HFD-LO and HFD-MO groups showed higher glycaemia (p < 0.05 versus NFD). However, no significant effect was observed on glycaemia, liver gluconeogenesis and liver ketogenesis when SO was replaced by either LO or MO. The body weight and the sum of epididymal, mesenteric, retroperitoneal and inguinal fat weights were higher (p < 0.05) in the HFD-SO and HFD-MO groups as compared with the NFD group. However, there was no significant difference in these parameters between the NFD and HFD-LO groups. Thus, the protective role of LO on lipid accumulation induced by an HFD rich in saturated fatty acid is potentially mediated by the high content of ɷ-3 polyunsaturated fatty acid in LO.

show abstract

“…A link between inflammation and insulin resistance has been proposed in recent years . In animal models, inhibition of TNF‐α, a major pro‐inflammatory cytokine, decreases insulin resistance and reduces hepatic gluconeogenesis . Non‐diabetic, non‐obese patients with inflammatory bowel disease treated with TNF‐α inhibitors exhibited a significant reduction in insulin, C‐peptide and insulin resistance index .…”

mentioning

confidence: 99%

Tumour necrosis factor‐alpha inhibitor induced recurrent symptomatic hypoglycaemia

Mah

Teng

Gilfillan

2019

Internal Medicine Journal

View full text Add to dashboard Cite

Infliximab treatment prevents hyperglycemia and the intensification of hepatic gluconeogenesis in an animal model of high fat diet-induced liver glucose overproduction

Abstract: The effect of infliximab on gluconeogenesis in an animal model of diet-induced liver glucose overproduction was investigated. The mice were treated with standard diet (SD group) or high fat diet (HFD group

Cited by 5 publications

References 16 publications

Molecular and pathophysiological relationship between obesity and chronic inflammation in the manifestation of metabolic dysfunctions and their inflammation‑mediating treatment options (Review)

Molecular and pathophysiological relationship between obesity and chronic inflammation in the manifestation of metabolic dysfunctions and their inflammation‑mediating treatment options (Review)

Effect of linseed oil and macadamia oil on metabolic changes induced by high‐fat diet in mice

Tumour necrosis factor‐alpha inhibitor induced recurrent symptomatic hypoglycaemia

Contact Info

Product

Resources

About