Link Between Hormones, Visceral Fat, And Intestinal Cancer

Data from a mouse-model study, published in Cancer Prevention Research, a journal of the American Association for Cancer Research, has found a direct causal link between visceral fat, the intra-abdominal fat cushioning the internal organs, and an increased risk for intestinal cancer.

Visceral fat accumulates in the abdominal cavity and is packed between the stomach, liver, intestines, kidneys, and other vital organs, providing protective padding. Epicardial fat is a form of visceral fat, surrounding the heart.

A visceral deposit is also a vital reserve of lipids, which can be metabolically burned to meet energy needs.

Visceral fat differs from subcutaneous fat, found just beneath the skin in the hypodermis – such as in the thighs and buttock regions – and intramuscular fat interspersed in skeletal muscle. Visceral fat is semi-fluid and is considered adipose tissue, unlike other forms of fat deposits.

Excess accumulation of visceral fat, where the belly is especially distended – called central obesity or “belly fat” – has been tied to the onset of type 2 diabetes, insulin resistance, and inflammatory disease. All very serious and preventable health conditions.

Due to hormonal differences, men are more prone to have fat amass in their belly. Women incur belly weight gain after menopause, otherwise estrogen encourages the fat to be stored in the thighs and buttocks.

Several epidemiological studies have suggested obese or overweight people are at an increased risk of developing numerous cancer types such as adenocarcinoma (glandular tissue) of the esophagus, colon cancer, breast cancer in postmenopausal women, endometrial cancer (lining of the uterus), and kidney cancer.

Derek M. Huffman, PhD – a postdoctoral fellow at the Institute for Aging Research at the Albert Einstein College of Medicine in Bronx, New York – and his team, focused primarily on the correlation of intestinal cancer to visceral fat.

According to Cancer.org, intestinal cancer (also known as small intestinal cancer) is a rare but pernicious form of the disease that germinates in the small intestines. US doctors diagnose about 1,200 malignant (life-threatening) small intestine tumors a year. Cancer is 50 times more common in the large bowel than in the small bowel.

The small intestine lies between the stomach and the colon and is about 20 feet long. The small intestine makes up more than 70 percent of the length and 90 percent of the surface area of the gastrointestinal (GI) tract. Its primary function is to digest and absorb nutrients.

There are four major types of small intestinal cancer. Carcinoid tumors, gastrointestinal stromal tumors, and lymphomas make up about 60 percent of small intestine cancer. Adenocarcinomas make up about 30 percent.

This type of cancer starts from the cells that line the intestine, developing much like colon cancer. It first begins as a small benign outgrowth called a polyp, and over time the polyp can change into a cancer. Most small intestinal cancers develop in the duodenum, the first part of the small intestine.

Huffman and his colleagues sought to determine if removing visceral fat in mice, genetically predisposed to develop colon cancer, might prevent or reduce the onset and growth of intestine-specific tumors.

Using a mouse-model to examine the influence of excessive visceral fat is ideal because mice have eight major deposits of anatomical adipose, four within the abdominal cavity, including a mesenteric deposit which forms a malleable glue-like web that supports the intestines.

Hormones, Visceral Fat, And Intestinal Cancer

The mice were arbitrarily assigned into three groups. One group ate an unrestricted diet throughout the entire study, rendering them obese. Additionally, they underwent a sham surgery – also known as a placebo surgery where the patient is anesthetized, incisions are made and stitched up, and the patient is restored to consciousness, giving the patient the illusion a procedure has been performed.

Another group were also permitted to gorge on an unrestricted diet and subsequently became obese, but had the actual visceral fat surgically excised. The third group was limited to a highly restricted diet, eating 60 percent of the caloric intake of the other two groups, reducing their overall visceral fat. They also underwent a sham surgery.

Huffman addressed the correlation of obesity and cancers saying, “There has been some skepticism as to whether obesity per se is a bona fide cancer risk factor, rather than the habits that fuel it, including a poor diet and a sedentary lifestyle.”

After evaluating the results of his study, Huffman determined, “Although those other lifestyle choices play a role, this study unequivocally demonstrates that visceral adiposity is causally linked to intestinal cancer.”

The researchers found the mice who underwent the sham surgeries who had the most body fat developed the greatest number of intestinal tumors, and overall had the highest mortality rate. Mice with the surgically removed or dietarily-reduced visceral fat both had a reduced presence of tumors.

It was a particularly intriguing finding, especially in the case of the obese mice who had the visceral fat removed versus the mice who were just on the restricted diet, as they were still overweight, they just had less abdominal fat.

When subdivided by gender, scientists noticed the female mice who underwent the fat removal procedure had a significantly notable reduction in tumors – more so than those who were calorically restricted.

However, in male mice the calorie restriction made more of an impact on decreasing the number of intestinal tumors. Removing the fat made little difference in comparison. This suggested important gender differences in how adiposity and nutrients interact with a tumor environment.

[Feature image via Shutterstock/Obese mouse Wikicommons]