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Word1Word2Word3 The Case of the Amazing Shrinking Fat Cell After using Lepti-Trim6 with leptin from Immune Tree, I can tell you that I have not only lost weight. I have also experienced a dramatic conversion of body mass from fat to muscle. Perhaps most noteworthy (and certainly delightful to this chocolate lover), is that my taste for sweets has been significantly blunted. Researchers say that is a beneficial property of this hormone-like protein. They’re right. sing the hormone-like messen- ger protein leptin to shrink your fat cells is an intriguing, potentially key new concept in weight loss. Diminishing the body’s cravings that lead to overeating is another criti- cal, new concept. And with more and more of us din- ing out on, or taking out, industrial- sized meal portions, it is clear that shrinking our fat cells and reducing cravings that lead to overeating are potentially two very good things. So what if we really could safely shrink our fat cells (without losing muscle)? What if we simply could safely lose the cravings that cause us to overeat? The science of slimming is now on the verge of such breakthroughs. We cannot assure everyone reading this report that the information we pre- sent will result in weight loss or con- version of fat to lean muscle, because the information is preliminary (and also individual biochemistry affects all outcomes). But, many of us welcome all the help we can get when it comes to appetite control and weight loss. Our mission is to keep you informed of cutting edge breakthroughs in health. Anecdotal reports are coming in now from individuals who are losing weight and/or becoming more trim with the use of a leptin-based colostrum formula from Immune Tree. It is called Lepti-Trim6. So we want to present this information. It may prove helpful to many of you. U that it is the combination of leptin and insulinlike growth factor-I (IGF-I) in colostrum that helps to create lean body mass,” says Fox, one of the world’s leading experts on colostrum, its formulation, utilization and applica- tions. Dr. Fox is scientific consultant to Immune Tree. “Leptin directs how you actually use fatty acids,” he continues. “Large fat cells indicate a leptin deficiency or an inability to properly use leptin due to faulty cell receptors or other feed- back mechanisms. It’s a vicious cycle. Once you get a lot of large fat cells you have inefficient uses of leptin and you end up with more fat cells and even more leptin because your body is no longer responding. But as people lose weight, their leptin levels decrease, making it difficult to reach ideal body weight. What we do know is that sup- plemental leptin seems to work.” Most telling is a 1999 study from the Journal of the American Medical Association that found that leptin not only resulted in significant weigh loss, “more than 95% of weight loss was fat loss,” note researchers. Meanwhile, researchers at the Howard Hughes Medical Institute have been using genechip technol- ogy—a powerful tool for analyzing the expression patterns of thousands of genes at a time—and have identified a number of genes that are specifically regulated by the hormone leptin. Identifying genes regulated by lep- tin will improve knowledge of how leptin causes its effects on weight and appetite, and may also offer new tar- gets for drugs designed to stimulate weight loss. Since the discovery of leptin in 1994, many have hoped that the hormone would be a promising weight-loss treatment for humans. Studies of the hormone’s weight- reducing effects in humans are underway, but researchers still have a way to go before they fully compre- hend how the hormone affects the brain and other tissues. In experiments described in the April 15, 2000, issue of the journal Genes & Development, Dr. Jeffrey M. Friedman, an HHMI investigator at The Rockefeller University, and Rockefeller colleagues Alexander Soukas, Paul Cohen and Nicholas D. Socci report that they are beginning to probe the genetic program orches- trated by leptin to induce weight loss. FYI Leptin Background Scientists Say Leptin Works As a longtime consultant to the dairy industry, Dr. Al Fox has seen firsthand the beneficial impact of leptin on body mass composition. “I have been involved in studies with lean body mass and calves, and we have demon- strated that supplemental colostrum aids lean body mass. It seems likely 36 The Doctors’ Prescription for Healthy Living / Volume 6, Number 6 Leptin, a hormone-like messenger protein (known technically as a cytokine), is produced in relatively large amounts by fat tissue and in smaller amounts by other peripheral organs, and then secreted into the bloodstream, where it travels to the brain and other tissues, causing fat loss and decreased appetite. Once leptin has been secreted by your fat cells, it travels to the hypothalamus—the part of your brain that has an influence on eating behavior. In the medial hypothala- mus, leptin activates “anorectic” nerve cells, which serve to suppress your appetite. At the same time, leptin prevents “orexigenic” cells from stimulating your appetite. Leptin (from the Greek leptos, meaning thin) first came to national attention in 1994 when the obesity gene and its product leptin were discovered. It was shown then that obese mice dropped 40 percent of their body weight after only one month of treatment with leptin. Leptin also improved symptoms of diabetes. Recently, the taste organ was found to be one of the peripheral targets for leptin. The hormone specifically inhibits sweet taste responses in lean mice. Thus, leptin appears to act as a modulator of sweet taste. Leptin also suppresses a gene that produces an enzyme known as acetyl-CoA carboxylase, or ACC, which is essential for fat production. When researchers injected laboratory mice with leptin, previously obese mice became as thin as rodent track stars. Some researchers believe that leptin works, in part, by inhibiting the synthesis of fat in fat cells and increasing the burning of fat in muscle cells—that it works at an enzymatic, cellular level. T H E L E P T I N FA C T O R c o n t i n u e d “We knew that an animal given lep- tin eats less and loses fat,” says Dr. Friedman. “And while restricting food intake also causes weight loss, we had reason to believe that the two weight- loss responses are very different.” For example, says Dr. Friedman, leptin triggers weight-loss of fat stores alone, while food-restriction robs the body of both fat and muscle. Also, he says, a diet-restricted human or animal com- pensates for decreased caloric intake by lowering energy expenditure, while leptin treatment shows no such energy-robbing effect. Until now, how- Most telling is a 1999 study from the Journal of the American Medical Association that found that leptin not only resulted in significant weight loss, “more than 95% of weight loss was fat loss,” note researchers. ever, no one had explored the molecu- lar basis of such differences in detail. Studying normal mice and a mutant strain that cannot produce leptin, the researchers looked for differences in gene expression patterns related to either leptin administration or caloric restriction. After administering leptin to or restricting food intake in the two groups of mice, the researchers ana- lyzed gene expression in the mice by extracting messenger RNA from their fat cells. Messenger RNA levels reflect the expression levels of different genes. They applied these collections of messenger RNA to a series of “oligonucleotide microarrays,” popu- larly known as genechips. Each kind of messenger RNA “found” and adhered to its corresponding gene on the genechip. Indicator molecules revealed the level of RNA present, showing the expression levels of hun- dreds of fat-tissue-related genes. Analyzing data from many such experiments with the mice, the scien- tists were able to group the expressed genes into clusters that appeared to behave similarly— increasing or decreasing in expression in tandem— as the mice were subjected to differ- ent regimes of leptin treatment or food restriction. “We were able to find at least half a dozen distinct clusters of genes that were specifically regulated by leptin and that were not regulated in the same way by food restriction,” says Dr. Friedman. “So, leptin is doing a lot more than just leading to food intake restriction.” The discovery of these leptin-regu- lated genes offers a glimpse of the complex metabolic machinery con- trolled by leptin. The new findings also open a promising pathway for understanding the complexity of lep- tin’s effects on different body tissues, said Friedman. Although researchers know that leptin is produced by fat cells and suppresses appetite by affecting the hypothalamus, the hor- mone-like protein may also trigger metabolic changes in fat and other tissues. Learning how changes in gene regulation lead to these effects is a goal of future studies in Friedman’s laboratory. Break Through Weight-loss Plateaus with Leptin The lowered levels of leptin associated with initial weight-loss may be offset by supplemental leptin. “No matter how hard you try, it’s often the case that losing the last 10 or 15 pounds of stubborn fat can take forever,” notes health writer Christian Finn. This is where supplemental leptin seems to help. In an experimental study, after two weeks of leptin treat- ment, leptin-deficient mice unable to produce leptin naturally lost 40 per- cent of their body weight. The reduced weight came exclusively from fat, mir- roring results from the human clinical trial. The body fat content of the nor- mal mice receiving leptin, however, also was reduced up to 12 percent. Food Consumption Reduced and Metabolic Rate Increased Leptin treatment not only reduced food consumption in the mice, but also increased their energy expenditure. Four days after starting leptin treat- ment, the mice with the deficient lep- tin production gene consumed about 60 percent less food compared to untreated mice. When the researchers put a group of untreated mice on a low calorie diet in which they were fed only as much food as the treated mice, the food- restricted mice lost less weight. This suggests that leptin also increases energy expenditure. In short, these early studies suggest that leptin is released from fat stores in response to a rise in fat stores—trig- gering appetite suppression and an increase in energy expenditure. Thus, says one weight-loss expert, “Think of leptin a little like a thermostat—reduc- ing food intake and increasing the metabolic rate when your body fat moves beyond a set point.”
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