What is the clinical evidence from this study?

Study design: Case-Control. Population: Obesity and Colon Carcinoma (n=71). Intervention: Obesity and Colon Carcinoma vs. Normal weight without colon carcinoma. Primary outcome: IL1B gene expression levels in visceral adipose tissue and colon (p=<0.01).

September 21, 2024Journal of Physiology and Biochemistry10 citationsOpen Access

Increased expression of IL-1β in adipose tissue in obesity influences the development of colon cancer by promoting inflammation

Q: What are the key findings of this study?

Obesity and colon carcinoma significantly upregulated the transcript levels of IL1B in visceral adipose tissue and colon tissue.

GNGabriela Neira JGJavier Gómez‐Ambrosi JCJavier A. Cienfuegos

Key Result

Obesity and colon carcinoma significantly upregulated the transcript levels of IL1B in visceral adipose tissue and colon tissue.

Study Design

Type

Case-Control (n=71)

Multicenter

Structured PICO

Does obesity and colon cancer affect the expression of IL-1β, and does IL-1β or adipocyte-conditioned medium promote inflammation in colon cancer cells?

Population

71 human volunteers (24 normal-weight [13 with colon cancer], 47 with obesity [13 with colon cancer]), 38 eight-week-old male Wistar rats (diet-induced obesity model), and HT-29 colorectal adenocarcinoma cell line.

Intervention

In rats: sleeve gastrectomy or caloric restriction (pair-fed). In HT-29 cells: treatment with IL-1β (1, 10, 100 ng/mL) or adipocyte-conditioned medium (ACM) (20% and 40%) from patients with obesity.

Comparator

In humans: Normal weight without CC vs Obesity without CC vs Normal weight with CC vs Obesity with CC. In rats: Sham surgery or normal diet. In cells: Control (untreated).

Outcome

Expression levels of IL1B in visceral adipose tissue and colon tissuesurrogate

IL-1β expression is increased in visceral adipose tissue and colon tissue in obesity and colon cancer, promoting a pro-inflammatory environment that may contribute to tumor development.

Main Result

p-value: p=<0.01

Limitations

Further cell lines should be used under the same conditions to further amplify findings.
Determination of the circulating levels of IL-1β in the animal model is needed to better elucidate the role of weight loss.
Measurement of protein expression levels is needed to shed information about full protein functionality.

Abstract

Excess adiposity contributes to the development of colon carcinoma (CC). Interleukin (IL)-1β is a pro-inflammatory cytokine relevant in obesity-associated chronic inflammation and tumorigenic processes. We herein aimed to study how obesity and CC affects the expression of IL1B, and to determine the impact of IL-1β on the regulation of metabolic inflammation and gut barrier function in the context of obesity and CC. Samples from 71 volunteers were used in a case-control study and a rat model of diet-induced obesity (DIO). Furthermore, bariatric surgery was used to determine the effect of weight loss on the intestinal gene expression levels of Il1b. To evaluate the effect of IL-1β and obesity in CC, we treated the adenocarcinoma cell line HT-29 with IL-1β and the adipocyte-conditioned medium (ACM) from patients with obesity. We showed that obesity (P < 0.05) and CC (P < 0.01) upregulated the transcript levels of IL1B in visceral adipose tissue as well as in the colon from patients with CC (P < 0.01). The increased expression of Il1b in the ileum and colon in DIO rats decreased after weight loss achieved by either sleeve gastrectomy or caloric restriction (both P < 0.05). ACM treatment on HT-29 cells upregulated (P < 0.05) the transcripts of IL1B and CCL2, while reducing (P < 0.05) the expression of the anti-inflammatory ADIPOQ and MUC2 genes. Additionally, IL-1β upregulated (P < 0.01) the expression of CCL2 and TNF whilst downregulating (P < 0.01) the transcript levels of IL4, ADIPOQ and TJP1 in HT-29 cells. We provide evidence of the important role of IL-1β in obesity-associated CC by directly promoting inflammation.

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