My science is about appetite regulation. It is clear that human body is well adapted to energy deficiency, when food is scarce. We then get hungry and seek for food. Today there is an excess of palatable food present at low prize the day around. Our body is not adapted to this and cannot resist overeating. The satiety signals are overridden by the strong reward given by modern processed food. To stay in appetite control we must therefore fortify the satiety signals.
I have long been working to understand how satiety is expressed. It is clear that satiety has two parts 1) filling of the stomach and 2) central satisfaction. Modern processed food is energy-rich, i.e. has many calories in a small volume. Therefore filling of the stomach is not fulfilled. Second, modern food is rapidly digested in the intestine. Satiety signals are released as long as food stays in the intestine. Therefore satiety is weak with modern processed food. Natural food like fruit, berries and vegetables are space filling and also slowly digested in the intestine. They therefore give strong satiety. It is easier to get in energy balance with such food.
My special interest has been in intestinal fat digestion. My doctoral thesis was about “Fat digestion in the intestine by pancreatic lipase and colipase”. The main enzyme responsible for intestinal fat digestion is pancreatic lipase. It needs colipase to be active in the intestine where bile salt is present to emulsify the dietary fat. Colipase is absolutely necessary to have any fat digestion in the intestine.

I came into the field of appetite regulation when working with pancreatic colipase. I found that colipase was released as procolipase, which produced a peptide to become the active colipase. The peptide was named enterostatin and turned out to act as a satiety signal with specificity for fat. Enterostatin displayed many activities, like reducing cholesterol levels, decreasing insulin secretion and increasing thermogenesis. When given to man it was not powerful enough to promote satiety. This made me widen my views on appetite regulation. One signals is not enough, there needs to be several at the same time.

Working with colipase-/- animals demonstrated that these were smaller than their normal littermates. I then came to think that fat digestion is important to control the appetite and body weight. We found a molecule, diethyl ether that actually slowed down fat digestion by pancreatic lipase/colipase. When given to experimental animals they decreased their food intake and had increased satiety signals. Theses experiments demonstrated that a retarded fat digestion gave an increased satiety, without leading to steatorrea or fatty stools. I did not like the idea of giving synthetic products for the control of appetite. I wanted to find something that was natural and accepted by the body as a natural product.

The next step was now to find something that slowed down intestinal fat digestion and that was itself degraded in the intestine without any rest product. I thought of galactolipids, which are present in plants, and known to reduce the rate of intestinal fat digestion. I told this to my husband Per-Åke Albertsson, professor in Biochemistry, Lund University. And then he said: Why don´t you try thylakoids? They contain lots of galactolipids.

Good. This was immediately investigated in my laboratory the next day. They had a powerful inhibiting effect on pancreatic lipase/colipase during fat digestion. When given to animals they promoted the release of satiety hormones and promoted reduced body weight. In human they promoted the release of the satiety signal cholecystokinin, known to promote satiety for fat and protein.

Further experiments demonstrated that thylakoids dampened hunger signals in human and also the subjective rating of hunger. Glucose levels were found more balanced and stable. A third effect was the change of the intestinal micro biota with an increase of healthy bacteria like the Lactobacillus Reuteri.

The mechanism of thylakoids seems to involve several different processes. One is the binding of thylakoids to fat droplets; another is the binding to pancreatic lipase and colipase, thereby slowing down fat digestion. The thylakoids are themselves eventually broken down and therefore do not yield any rest product. The thylakoids also filter glucose absorption in the intestine, to give a more low-glycaemic glucose uptake. Balanced blood glucose is important to keep appetite control. The change in bacteria flora may be important to explain the lipid-lowering effect of thylakoids. My research group consists of Caroline Montelius, Karolina Östbring, Nadia Osman and Eva-Lena Stenblom. I work in close collaboration with Mona Landin-Olsson, Per-Åke Albertsson, Sinan Emek and Björn Weström.

My research is supported by Swedish Medical Research Council, by FORMAS, by Region Skåne, by Vinnova and by Royal Physiographic Society.