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Hydroxycitric Acid Delays Intestinal Glucose Absorption; Indirect Insulin/Sugar Effect Could Point To Therapeutic Effect

Mechanism mirrors ‘South Beach Diet’ dictum: level the sugar peaks to reduce cravings, insulin surplus

BETHESDA, Md. (May 18, 2005) – In this obesity-obsessed world, the dream ingredient must be something that tastes good enough to be a condiment or flavoring and yet somehow helps us keep our weight down. Consider hydroxycitric acid (HCA), known variously as Brindle berry or Malabar tamarind, which is used in Indian and Thai food as a condiment and flavoring agent.

In Indian folk medicine as a dried powder or tea it’s indicated as a laxative and for rheumatism. As Malabar tamarind, it can substitute for lime, and in Ceylon it’s used along with salt to cure fish.

For HCA, though, the other half of the taste-benefit formula is much less clear. Animal studies suggest HCA may reduce food intake followed by weight loss, but no controlled human trials have shown either effect. Nevertheless, many people seem to believe HCA will help them lose weight. It’s sold by vitamin and other specialty shops as Citrimax or Citrin, and is a featured ingredient in such dietetic aids as Herbalife’s “Snack Defense” tablets.

A group of Dutch researchers went back to basics and studied how and if HCA affects glucose absorption, a key component of metabolism. The study, entitled “Hydroxycitric acid delays intestinal glucose absorption in rats,” appears online and in the June issue of the American Journal of Physiology-Gastrointestinal and Liver Physiology, published by the American Physiological Society. The research was conducted by Peter Y. Wielinga, Renate E. Wachters-Hagedoorn, Brenda Bouter, Theo H. van Dijk, Frans Stellaard, Arie G. Nieuwenhuizen, Henkjan J. Verkade, and Anton J.W. Scheurink.

HCA strongly delays post-meal glucose levels, reducing insulin output

In the study, rats were administered HCA prior to “mimicking a meal by infusing sugar into the stomach,” explained lead author Wielinga. “Compared with controls, which had no HCA, the test rats’ rise in blood sugar was much slower, but over 2 ½ hours all the sugar was absorbed.”

In addition, “HCA strongly attenuated postprandial (after-meal) blood glucose levels after both intragastric (or IG, into the stomach, at P < 0.01) and intraduodenal (or ID, into the small intestine, at P < 0.001) glucose administration” which also excluded the possibility of "a major effect of HCA on gastric emptying,” the paper stated. “These data support a possible role for HCA as a food supplement in lowering postprandial glucose profiles,” it said.

Wielinga said that the absorption delay was significant because “sugar that is normally absorbed rather quickly -- within about 20 minutes -- took over 2 hours after HCA ingestion. This delay is good because it reduces the high peaks of glucose, which otherwise would require the body to produce a lot of insulin to deal with the ‘meal.’

“Finding this delayed absorption is a completely new phenomenon and one that might be useful to follow up: why is it delayed and how might this affect humans?” Wielinga reported. But he warned that “we don’t know how this will translate into humans. Care must be taken because the comparable dosage we use in rats is probably way too high for humans,” he added.

The ‘South Beach’ inference; speculation about HCA’s potential in diabetes

One of the tenets of the successful “South Beach Diet” is to reduce and slow sugar absorption. In his first book, Dr. Arthur Agatston explains: “What we’re concerned with here is the speed with which our bodies get at the sugars….If the body experiences a fast infusion of sugars, a lot of insulin is required. If the sugars are metabolized more slowly, the insulin is released gradually. This is a crucial difference, as far as obesity is concerned: Fast sugar is worse for you; slower is better.”

Besides the implication for extra sugar being stored (as fat) rather being used effectively, Dr. Agatston notes that with large sugar infusions, the body often produces too much insulin, which then lowers the blood sugar level. When that happens, he writes, “new cravings are created, requiring more quick carbohydrate fixes.”

Next steps

Wielinga again warned that any comparison between rats and humans regarding HCA have to be treated very carefully. However, he said now that it is known where HCA has an effect in rats, the next step is to try and uncover its mechanism. He said that “if we can reduce the peaks and valleys of insulin with HCA, then it might have some application in diabetes, both in slowing progression to diabetes 2 and since these people have an obesity problem, it could potentially have an additional benefit in the therapeutic field. But this is all highly speculative,” Wielinga added.

Wielinga, who is moving to the Institute of Veterinary Physiology at the University of Zurich, Switzerland, said another promising area “we plan to study is HCA’s affect on food intake reduction, since it is known that HCA seems to reduce some food intake in rodents.”

Source and funding

The study, entitled “Hydroxycitric acid delays intestinal glucose absorption in rates,” appears online and in the June issue of the American Journal of Physiology-Gastrointestinal and Liver Physiology, published by the American Physiological Society.

The research was conducted by Peter Y. Wielinga, Brenda Bouter, and Anton J.W. Scheurink of the Dept. of Neuroendocrinology, University of Groningen, Haren, the Netherlands; Renate E. Wachters-Hagedoorn, Theo H. van Dijk, Frans Stellaard and Henkjan J. Verkade of the Center for Liver, Digestive and Metabolic Diseases, Dept. of Pediatrics, University Hospital, Groningen; and Arie G. Nieuwenhuizen of Numico Research, Wageningen.

Partial funding for this research came from Dutch Ministry of Economic Affairs doctoral grant and the University of Groningen (Wielinga).

Editor’s note: A copy of the research paper by Wielinga et al. is available to the media. Members of the media may obtain an electronic version and interview members of the research team by contacting Donna Krupa at the American Physiological Society, (301) 634-7209, cell (703) 967-2751 or dkrupa@the-aps.org.

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