Relationship between IGF-1 and body weight in inflammatory bowel diseases: Cellular and molecular mechanisms involved

Guijarro, Luis; Cano-Martínez, D.; Toledo-Lobo, M Val; Salinas, Patricia Sanmartín; Chaparro, María; Gómez-Lahoz, Ana M.; Zoullas, Sofia; Rodríguez-Torres, Rosa; Domingo, Alberto; Monasor, Laura Sebastián; Ruiz, Lı́dia; Boyano‐Adánez, María del Carmen; Guerra, Iván; Iborra, Marisa; Cabriada, José Luis; Bujanda, Luís; Taxonera, Carlos; García–Sánchez, Valle; Marín-Jiménez, Ignacio; Acosta, Manuel Barreiro‐de; Vera, Isabel; Martín-Arranz, María Dolores; Mesonero, Francisco; Sempere, Laura; Gomollón, Fernando; Hinojosa, Joaquín; Álvarez‐Mon, Melchor; Gisbert, Javier P.; Ortega, Miguel A.; Hernández-Breijo, Borja

doi:10.1016/j.biopha.2021.112239

Cited by 14 publications

(5 citation statements)

References 37 publications

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“…Moreover, the rate of low BMI in patients who did not receive anti-TNF therapy was approximately 2.5 times higher than that in those who received anti-TNF therapy (40.73% versus 19.72%). A recent study discovered that insulin-like growth factor-1 (IGF-1) in the serum of adult CD patients was downregulated by adalimumab and that IGF-1 treatment contributed to the restoration of the mucosal barrier, attenuating weight loss and shortening of the colon ( 24 ), which may explain the retention of lean mass by anti-TNF therapy.…”

Section: Discussionmentioning

confidence: 99%

Earlier anti-TNF therapy reduces the risk of malnutrition associated with alterations in body composition in patients with Crohn’s disease

Wang

Yao²,

He³

et al. 2023

Front. Nutr.

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BackgroundAnti-TNF therapy has been found to exert an influence on long-term nutritional status and even reverse malnutrition in patients with Crohn’s disease.Aimsto observe the effect of anti-TNF therapy on nutritional status in patients with Crohn’s disease, investigate the correlation between the timing of anti-TNF therapy and the human body composition and examine independent body composition factors for predicting malnutrition in these patients.MethodsThis was a retrospective study of 115 patients with Crohn’s disease. Body composition parameters were assessed by bioelectrical impedance analysis. The nutritional status of the patients was determined by NRS2002 and MNA.ResultsThe BMI, BFMI, FFMI, BCMI, SMI, BMC, intracellular water, protein and BMR were significantly lower in patients without any biologic agents (p < 0.05). Negative correlations were found between BMC, intracellular water, extracellular water, protein and BMR and the interval between the first symptom and first dose by Spearman’s correlation analysis (r < 0, p < 0.05). Low BMI (OR 0.602, 95% CI 0.434–0.836, p = 0.002), low FFMI (OR 0.678, 95% CI 0.507–0.906, p = 0.009), and low BCMI (OR 0.564, 95% CI 0.367–0.868, p = 0.009) were independent risk factors for malnutrition in Crohn’s disease patients. Anti-TNF therapy tended to reduce the malnutrition probability as assessed by Cox regression analysis (OR: 0.217, 95% CI 0.057–0.821, p = 0.024).ConclusionBody composition analysis is predictive of malnutrition in patients with Crohn’s disease. Early application of anti-TNF therapy significantly affected skeletal muscle mass, fat mass and bone mineral content, supporting their long-term nutritional status and reducing their probability of malnutrition.

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Section: Discussionmentioning

confidence: 99%

Earlier anti-TNF therapy reduces the risk of malnutrition associated with alterations in body composition in patients with Crohn’s disease

Wang

Yao²,

He³

et al. 2023

Front. Nutr.

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“…This study was conducted to investigate the effects of high dietary iron supplementation on intestinal injury and intestinal repair function, especially for ISCs in the jejunum and colon of adult mice. The symptoms of DSS-induced colitis are weight loss ( 31 ), disruption of the gut index ( 32 ) and morphology, and damage to intestinal stem cells ( 33 ). In vitro organoid cultures were used to observe the regulation of ISC compartments after tissue injury ( 34 ).…”

Section: Discussionmentioning

confidence: 99%

Dietary High Dose of Iron Aggravates the Intestinal Injury but Promotes Intestinal Regeneration by Regulating Intestinal Stem Cells Activity in Adult Mice With Dextran Sodium Sulfate-Induced Colitis

et al. 2022

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The effects of excessive dietary iron intake on the body have been an important topic. The purpose of this study was to investigate the effects of high-dose iron on intestinal damage and regeneration in dextran sodium sulfate (DSS)-induced colitis model mice. A total of 72 8-week-old adult C57BL/6 mice were randomly divided into two dietary treatment groups: the basal diet supplemented with 45 (control) and 450 mg/kg iron (high-iron) from ferrous sulfate. The mice were fed different diets for 2 weeks, and then 2.5% DSS was orally administered to all mice for 7 days. Samples of different tissues were collected on days 0, 3, and 7 post administration (DPA). High-iron treatment significantly decreased the relative weight of the large intestine at 7 DPA but not at 0 DPA or 3 DPA. High dietary iron increased the jejunal villus width at 0 DPA, decreased the villus width and the crypt depth of the jejunum at 3 DPA, and decreased the number of colonic crypts at 7 DPA. Meanwhile, high dietary iron decreased the number of goblet cells in the jejunal villi and the Paneth cells in the jejunal crypts at 0 DPA, increased the number of goblet cells per crypt of the colon at 3 DPA, and the number of Paneth cells in the jejunal crypts, the goblet cells in the colon, the Ki67-positive proliferating cells in the colon, and the Sex-determining region Y-box transcription factor 9+ (SOX9) cells in the jejunum crypts and colon at 7 DPA. The organoid formation rate was increased by high-iron treatments at 3 DPA and 7 DPA. High dietary iron treatment decreased the mRNA level of jejunal jagged canonical Notch ligand 2 (Jag-2) at 0 DPA and bone morphogenetic protein 4 (Bmp4) and neural precursor cell-expressed developmentally downregulated 8 (Nedd8) in the jejunum and colon at 7 DPA, whereas it increased the mRNA expression of the serum/glucocorticoid-regulated kinase 1 (Sgk1) in the colon at 3 DPA. The results suggested that a high dose of iron aggravated intestinal injury but promoted intestinal repair by regulating intestinal epithelial cell renewal and intestinal stem cell activity in adult mice with colitis.

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“…A recent multicenter study in IBD patients showed a reduction in serum IGF-1 levels in the prolonged treatment of adult CD patients with adalimumab (anti-TNF-α mAbs). The role of not only GH, but also the impact of ghrelin on GH secretion, and the effect of TNF-α blockade on GH and IGF-1 production in CD treatment with these antibodies were discussed [ 71 ].…”

Section: Igf Signaling and Colorectal Cancer—a Brief Summarymentioning

confidence: 99%

“…Similarly, the beneficial effects of IGF-1 on biochemical (e.g., glucose, albumin and total protein levels) and clinical (e.g., maintenance of normal colon size, maintenance of normal body weight and lean mass) and histological (restoration of the mucosal barrier) parameters were demonstrated in experimental DSS-induced colitis in rats. These changes were explained by the re-sensitization of the IGF-1/IRS-1/AKT pathway to exogenous IGF-1 [ 71 ].…”

Section: Autophagy In Normal Large Intestine Epithelial Cells—implica...mentioning

confidence: 99%

Autophagy and the Insulin-like Growth Factor (IGF) System in Colonic Cells: Implications for Colorectal Neoplasia

Kasprzak

2023

IJMS

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Colorectal cancer (CRC) is one of the most common human malignancies worldwide. Along with apoptosis and inflammation, autophagy is one of three important mechanisms in CRC. The presence of autophagy/mitophagy in most normal mature intestinal epithelial cells has been confirmed, where it has mainly protective functions against reactive oxygen species (ROS)-induced DNA and protein damage. Autophagy regulates cell proliferation, metabolism, differentiation, secretion of mucins and/or anti-microbial peptides. Abnormal autophagy in intestinal epithelial cells leads to dysbiosis, a decline in local immunity and a decrease in cell secretory function. The insulin-like growth factor (IGF) signaling pathway plays an important role in colorectal carcinogenesis. This is evidenced by the biological activities of IGFs (IGF-1 and IGF-2), IGF-1 receptor type 1 (IGF-1R) and IGF-binding proteins (IGF BPs), which have been reported to regulate cell survival, proliferation, differentiation and apoptosis. Defects in autophagy are found in patients with metabolic syndrome (MetS), inflammatory bowel diseases (IBD) and CRC. In neoplastic cells, the IGF system modulates the autophagy process bidirectionally. In the current era of improving CRC therapies, it seems important to investigate the exact mechanisms not only of apoptosis, but also of autophagy in different populations of tumor microenvironment (TME) cells. The role of the IGF system in autophagy in normal as well as transformed colorectal cells still seems poorly understood. Hence, the aim of the review was to summarize the latest knowledge on the role of the IGF system in the molecular mechanisms of autophagy in the normal colon mucosa and in CRC, taking into account the cellular heterogeneity of the colonic and rectal epithelium.

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Relationship between IGF-1 and body weight in inflammatory bowel diseases: Cellular and molecular mechanisms involved

Cited by 14 publications

References 37 publications

Earlier anti-TNF therapy reduces the risk of malnutrition associated with alterations in body composition in patients with Crohn’s disease

Earlier anti-TNF therapy reduces the risk of malnutrition associated with alterations in body composition in patients with Crohn’s disease

Dietary High Dose of Iron Aggravates the Intestinal Injury but Promotes Intestinal Regeneration by Regulating Intestinal Stem Cells Activity in Adult Mice With Dextran Sodium Sulfate-Induced Colitis

Autophagy and the Insulin-like Growth Factor (IGF) System in Colonic Cells: Implications for Colorectal Neoplasia

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