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According to a Study

Certain Intestinal Bacteria Causes Sugar Cravings

Woman craves sugar - caused by an intestinal bacterium
If you often feel an excessive craving for sugar, the cause could be in your gut Photo: Getty Images

January 27, 2025, 4:48 pm | Read time: 4 minutes

The gut microbiome is a key element for general health and the functioning of various bodily processes. Among other things, it also plays a role in controlling body weight. In this context, researchers have now gained exciting insights into the influence of a specific gut bacterium on blood sugar levels – and you probably already guessed that there is a connection here with eating behavior. FITBOOK author Laura Pomer explains the details of the study.

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From digestion, hormone production, and brain function to the immune system, the gut microbiome, i.e., the entirety of microorganisms in the gut, plays a key role in a wide range of important bodily functions. When it comes to weight control, it is worth mentioning that the microbiome controls fat and sugar metabolism, among other things. Of course, it is also true that diet has a decisive influence on this process. However, as a new study has now shown, a specific intestinal bacterium also plays a role – particularly with regard to sugar cravings.1

Study on the Influence of Gut Bacteria on Weight Control

It was already known that the ability to control weight and the appetite for certain foods can be linked to signals from the gut. Years ago, FITBOOK reported on a study according to which the composition of intestinal bacteria can determine weight loss success.2 Prevotella and Bacteroidetes bacteria, in particular, had a favorable influence. They are said to be able to utilize absorbed nutrients more efficiently and thus reduce the body’s calorie intake. The less successful slimmers among the test subjects lacked the aforementioned microorganism.

The new study looked specifically at the intestinal bacterium Bacteroides vulgatus and its influence on sugar cravings. This is because it can be one of the main causes of weight gain and the development of the metabolic disorder type 2 diabetes. In moderation, the desire for sugar is normal in evolutionary terms. It provides energy and thus, put simply, keeps us alive. But what exactly is the reason why the craving is much stronger in some people than in others? The research team looked for answers to this question in the intestines of both humans and mice diagnosed with diabetes.

Lack of a Certain Intestinal Bacterium Causes Sugar Cravings

60 type 2 diabetes patients and 18 laboratory animals were included in the analysis. When compared with healthy control groups, the researchers found fewer intestinal bacteria of the Bacteroides vulgatus type in the test subjects’ blood. This resulted in a reduced occurrence of the metabolic product pantothenate. Pantothenate plays a central role in the regulation of blood sugar levels. As a reminder, a drop in blood sugar levels can cause sugar cravings.

The connections do not stop here. As the researchers explain, one of the tasks of pantothenate is to stimulate the production of FFAR4. As part of the study, they specifically added pantothenate to the test subjects. This led to a stimulation of FFAR4 release. FFAR4 stands for “free fatty acid receptor 4” and is mainly found in (human and animal) fat cells. However, it is also found in immune cells and blood vessel cells. The receptor influences metabolic processes as it promotes the release of hormones such as GLP-1 (glucagon-like peptide-1). The reduced presence of pantothenate in the test subjects was also associated with a reduced presence of FFAR4 and with corresponding consequences for the release of the hormone GLP-1 in the intestine.

GLP-1, Known from the “Weight Loss Injection”

Now, you’ve probably pricked up your ears. The hormone GLP-1 is important for blood sugar regulation and the feeling of satiety. You have recently read more about it in connection with the so-called “weight loss injection.” GLP-1-based drugs (e.g., Ozempic and Wegovy) were originally used to treat diabetes and have now been used for some time to treat obesity with medication due to their appetite-suppressing effect. The therapy is effective – but after discontinuation, the weight returns to its previous state in the majority of patients. It would, therefore, be all the more interesting to find gentler methods to increase GLP-1 release.

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Possible Significance of the Results

The findings of the study could provide the basis for new treatments for both obesity and metabolic diseases. One approach would be to specifically stimulate the intestinal flora with a focus on the intestinal bacterium Bacteroides vulgatus in order to effectively regulate the appetite for sugar. In other words, to imitate the undisputed effect of the weight loss injection minus the side effects associated with it. For example, based on the findings, it would be conceivable to recommend the consumption of selected probiotics – those rich in pantothenic acid – for the treatment or prevention of type 2 diabetes and, thus, also for weight control.

But it is still too early for this. The study authors emphasize that further extensive clinical research is needed to develop a precise understanding of the mechanisms. The current study is based on too little data to draw reliable conclusions about the success of the therapy. It is also questionable to what extent the findings obtained in mice can be transferred to humans.

This article is a machine translation of the original German version of FITBOOK and has been reviewed for accuracy and quality by a native speaker. For feedback, please contact us at info@fitbook.de.

Topics Abnehmen Darmgesundheit Diabetes mellitus Typ 2 Übergewicht

Sources

  1. Zhang T., Wang W., Li J. et al. (2025), Free fatty acid receptor 4 modulates dietary sugar preference via the gut microbiota. Nature ↩︎
  2. Gibbons SM, Diener C, Qin S et al (2021). Baseline Gut Metagenomic Functional Gene Signature Associated with Variable Weight Loss Responses following a Healthy Lifestyle Intervention in Humans. mSystems ↩︎
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