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Acetate Has a Potential Role in Obesity and Metabolic Syndrome

Certain gut bacteria are more common in obese people and those with metabolic syndrome.

Although the health relevance of this is not completely understood, many scientists believe that an imbalanced gut microbiota (dysbiosis) may contribute to obesity and metabolic syndrome.

Growing evidence suggests that certain chemical compounds produced by gut bacteria play a role. These include short-chain fatty acids, such as butyrate, propionate and acetate.

Below is a detailed summary of a recent study on the potential role of acetate in the development of obesity.

Acetate

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This was a series of experiments in rats investigating the potential role of acetate in the development of obesity and metabolic diseases.

Acetate mediates a microbiome-brain-β-cell axis to promote metabolic syndrome.

Finding 1: A High-Fat Diet Increased Acetate Levels

The researchers discovered that a high-fat diet increased circulating acetate levels and whole-body acetate turnover in rats. It also more than doubled the levels of acetate in the cecum and colon.

Colon removal, colon washout or a broad-spectrum antibiotic treatment reduced whole-body acetate turnover by 75–90%.

Additionally, the study showed that rats without any gut bacteria had negligible amounts of acetate in their digestive tracts.

Together, these findings strongly suggest that acetate-producing bacteria in the colon were responsible for the rise in acetate.

In rats that had been fed a high-fat diet for 4 weeks, a 48-hour fast led to a 50% reduction in whole-body acetate turnover. In contrast, calorie excess increased acetate turnover.

Therefore, it seems that acetate production is driven by calorie-dense diets.

In a separate test-tube experiment, the researchers showed that bacteria in feces can produce acetate from glucose or fatty acids.

Bottom Line: A high-fat diet may increase intestinal and circulating acetate levels.

Finding 2: Acetate Increased Insulin Secretion

The researchers detected a significant increase in glucose-stimulated insulin secretion (GSIS) in rats fed a high-fat diet for 3 days or 4 weeks.

Injections of acetate into rats fed a normal diet led to similar increases in GSIS, indicating that acetate was responsible for the effects.

Interestingly, the increase in GSIS was blocked after colon removal, colon washout or a broad-spectrum antibiotic treatment.

Taken together, these findings strongly suggest that elevated bacterial production of acetate in the colon is responsible for the increased GSIS.

Bottom Line: A high-fat diet or increased acetate production in the colons of rats led to increases in glucose-stimulated insulin secretion.

Finding 3: Acetate Affects Insulin Levels Via the Parasympathetic Nervous System

Instead of directly affecting the pancreas, the study indicates that acetate affects insulin levels indirectly through the parasympathetic nervous system (PNS).

The researchers measured a marker of PNS activity or gastrin, a digestive hormone whose levels are known to be under PNS control.

After injecting rats with acetate for one hour, circulating gastrin levels increased threefold, indicating increased PNS activity.

Additionally, acetate levels in the brain increased, confirming that acetate is able to cross the blood-brain barrier and enter the brain circulation.

The brain communicates with the gut via the vagus nerve, which is part of the PNS. When the researchers severed the vagus nerve, acetate’s effects on insulin levels stopped and insulin levels reduced fourfold.

The researchers got similar results when they injected the rats with atropine, a chemical that blocks the activity of the PNS and vagus nerve.

These findings strongly suggest that acetate affects insulin levels indirectly via the brain and PNS.

Bottom Line: Acetate affects insulin levels via the brain and parasympathetic nervous system.

Finding 4: Chronically Elevated Acetate Promotes Weight Gain and Metabolic Disease

The researchers also investigated the effects of continuously injecting acetate into the stomach for 10 days. The amount of acetate used mimicked the effects of a high-fat diet.

Doing this increased the following metabolic factors:

  • Insulin secretion.
  • Insulin resistance.
  • Ghrelin levels: Acetate caused a threefold increase in the levels of ghrelin, the hunger hormone.
  • Triglycerides: Acetate increased the levels of triglycerides in the liver and muscles.
  • Liver gluconeogenesis: Formation of sugar increased in the liver.

Acetate also doubled the rats’ calorie intake and weight gain during the 10-day study period, an effect largely explained by the rise in ghrelin.

All of these effects were blocked when the researchers severed the vagus nerve, suggesting that acetate affects metabolism indirectly via the brain and parasympathetic nervous system.

Although acetate may increase appetite, previous studies indicate propionate (another short-chain fatty acid) reduces calorie intake and the appeal of high-calorie foods.

Bottom Line: Injecting acetate into the stomach for 10 days led to increased calorie intake and promoted weight gain and metabolic disorders.

Limitations

These studies were done in rats.

Although basic metabolism is similar in rats and humans, the findings need to be confirmed in clinical trials.

Summary and Real-Life Application

This series of experiments in rats suggests acetate, which is formed by gut bacteria in response to calorie-dense foods, may promote obesity and metabolic disease.

Although a number of lifestyle factors contribute to obesity and metabolic syndrome, this study strongly suggests that the gut microbiota may play an important role.

However, before any solid conclusions can be reached about the role of acetate in humans, clinical trials need to confirm the findings of the current study.

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