Category: diet


We investigated the effects of PGC-1α (peroxisome proliferator-activated receptor γ coactivator-1α) overexpression on the oxidative capacity of human skeletal muscle cells ex vivo. PGC-1α overexpression increased the oxidation rate of palmitic acid and mRNA expression of genes regulating lipid metabolism, mitochondrial biogenesis, and function in human myotubes. Basal and insulin-stimulated deoxyglucose uptake were decreased, possibly due to upregulation of PDK4 mRNA. Expression of fast fiber-type gene marker (MHCIIa) was decreased. Compared to skeletal muscle in vivo, PGC-1α overexpression increased expression of several genes, which were downregulated during the process of cell isolation and culturing. In conclusion, PGC-1α overexpression increased oxidative capacity of cultured myotubes by improving lipid metabolism, increasing expression of genes involved in regulation of mitochondrial function and biogenesis, and decreasing expression of MHCIIa. These results suggest that therapies aimed at increasing PGC-1α expression may have utility in treatment of obesity and obesity-related diseases.


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To evaluate the efficacy and safety of high-dose α-lipoic acid in the treatment of diabetic polyneuropathy with regards to sensory symptoms and nerve conduction velocity.


A total of 236 diabetics with symptomatic polyneuropathy were enrolled into this 5-center, randomized, double-blind and placebo-controlled study of α-lipoic acid 1800 mg daily (n = 117) or matching placebo (n = 119) for 12 weeks. The primary outcome was total symptom score (TSS). Secondary end points included nerve conduction velocity, individual symptom score, HbA1c and safety parameters. The above parameters were reviewed and recorded at zero point and after treatment for 2, 4, 8, 12 weeks separately.


73.27% patients with symptomatic polyneuropathy improved after treatment with α-lipoic acid for 12 weeks versus 18.27% with placebo. TSS declined by 2.6 ± 2.3 with α-lipoic acid. And it was more than 0.7 ± 1.4 versus placebo (P < 0.05). TSS decreased quickly after treatment with α-lipoic acid for 2 weeks (P < 0.05). And it was better than placebo. Individual symptom scores of pain, extremity numbness, burning sensation or resting abnormal sensations were significantly diminished as compared to those before treatment and placebo group (all P < 0.05). Nerve conduction velocity had no change. HbA1c further decreased at the end of trial after α-lipoic acid treatment (P < 0.05). The incidence rates of adverse effects were 25.4% vs 11.8% in the treatment and control groups. The major manifestation was burning sensation from throat to stomach (12.7%).


Oral treatment with high-dose α-lipoic acid for 12 weeks may improve symptoms in patients with diabetic polyneuropathy. Dose of 600 mg thrice daily for 2 weeks has marked effects with a reasonable safety.

[PubMed – indexed for MEDLINE]


FAQs about Lipo-dissolve

Phosphatidylcholine/Deoxycholate Overview

What are lipo-dissolve injections?

Lipo-dissolve injections have become an increasingly popular means to remove excess fat. The procedure goes by many names (e.g., Lipostabil®, Lipodissolve, Flab-Jab, Lipojection, Lipotherapy, etc.) and involves the injection of mixtures of various chemicals into the fat through multiple microinjections administered over multiple treatment sessions. The desired end result is the gradual removal of localized fat deposits. Lipo-dissolve injections are generally not regarded by medical professionals to be as potent as liposuction, a powerful yet invasive surgical procedure in which multiple liters of fat are ‘sucked’ from patients in a single session. Lipo-dissolve therapy typically requires that dozens of small ‘fat burning’ injections of compounded phosphatidylcholine/deoxycholate (PCDC) be injected into fat and connective tissue over several sessions. These drugs are not FDA-approved.

What are the compounds/ingredients in the injectable solution?

The main compound used in lipo-dissolve is phosphatidylcholine (PC), a compound derived from soy that is a component of cell membranes in many organisms, including humans.1 Deoxycholate (DC), a naturally occurring bile salt produced by the liver, is also used in the formulation to solubilize phosphatidylcholine, thus keeping it in solution.1 Together, the main ingredients are commonly abbreviated as PCDC, however without a specific FDA-approved formulation for the injected solution, the ratio of the two compounds in a given formulation may be substantially different depending on the provider. Some providers also add small amounts of other medications, vitamins, and herbs. PCDC injections have not been approved by FDA for ANY indication and neither phosphatidylcholine nor deoxycholate are active ingredients in ANY FDA-approved drug.
Where do providers get the PCDC for lipo-dissolve injections?

The PCDC drug is obtained from compounding pharmacies, which traditionally make small quantities of unique drugs for specialized treatments (e.g., special versions of drugs for patients with allergic reactions). According to experts who discussed this issue with the Washington Post, in many situations involving compounded drugs, quality control and sterility can often be “spotty or nonexistent.”2
What is the standard lipo-dissolve procedure?

There is no standard process/procedure that has been studied in controlled clinical trials or to the satisfaction of the FDA. Therefore, the procedure will differ depending on the provider. FDA-approved drugs have a standardized drug formula and method of administration. With lipo-dissolve, individual providers determine dosing and technique. The lipo-dissolve procedure “typically” involves an average of 2-4 treatment sessions spaced 4-8 weeks apart.3According to the Aesthetic Surgery Journal, the maximum safe dose of PC is 100 mL per session with approximately 0.4 mL delivered with every micro-injection. However, because studies have not concluded a standard protocol outlining specific number of sessions, number of microinjections per session, and amount of PC needed for results, this average may vary greatly.4
How is the drug cleared from the body?

There is no scientific support for theories about how the drug is cleared from the body. It is unclear exactly how the body metabolizes and excretes the drug and the broken down fat cells. The injected chemicals are believed to trigger an inflammatory response as the fat cells are broken down and are thought to be excreted in the urine and feces. Without pharmacologic studies (those that study the compound’s mechanism of action and are required for FDA-approved drugs), these theories cannot be confirmed.
How long has the procedure been around? How many times has it been performed?

Cosmetic use of phosphatidylcholine injections was introduced at the First International Meeting of Mesotherapy in 1988 by Italian Physician Sergio Maggiori5. The formulation began being used for fat removal in Brazil in the 1990’s yet was later banned by ANVISA (Brazilian National Agency of Health Inspection). The procedure has only more recently been introduced in the U.S., and the American Society of Non-surgical Aesthetics estimates that 50,000 to 100,000 lipo-dissolve treatments have been performed in the USA and Europe6. Despite the numbers of treatments performed, the drug’s safety and efficacy cannot be confirmed without controlled clinical trials as required by the FDA.
I keep hearing different terms for the treatment (e.g., lipo-dissolve, advanced lipo-dissolve, lipotherapy, injection lipolysis, etc.), are they all the same thing?

The treatments are similar in that each typically involves the injection of an unapproved PCDC formulation.

What areas can be treated with injections?

Currently, people use PCDC in a variety of areas (chin, abdomen, thighs). However, no well-controlled studies have examined where in the body the drug may or may not work. There is no FDA-approval for this drug for any part of the body.

Does the phosphatidylcholine affect other cells in the body besides fat cells?

It is unknown whether the drug affects other cells in the body (such as muscle or nerve cells). While a “theory” has been proposed for the method by which phosphatidylcholine destroys fat cells, the scientific mechanism still is not well understood.7
Are the injections a proper treatment for weight loss?

Without FDA-approval, this answer is unknown. But according to lipo-dissolve providers, the answer is no. Lipo-dissolve is not a viable means to lose weight. The ideal candidate is at a healthy weight but possesses localized fat deposits that cannot be reduced by exercise and diet. Lipo-dissolve may be successful in reducing inches but may not show any reduction in actual weight.
Are the ingredients used for lipo-dissolve safe?

PCDC is an unapproved drug. According to physicians currently studying the procedure, “until more safety data becomes available, physicians may be placing patients at unknown risks as they become reliant upon a compounded formulation for these treatments.”8 Additionally, FDA has stated that “there are no FDA approved drugs with an approved indication to dissolve fat and FDA cannot assure the safety and efficacy of these types of drugs.”8

FDA Status
Is the drug approved by the FDA?

PCDC is not approved by the FDA for any use. Furthermore, neither PC nor DC alone are active ingredients in any FDA-approved drug. FDA has issued a statement warning consumers “there are no FDA-approved drugs with an approved indication to dissolve fat and FDA cannot assure the safety and efficacy of these types of drugs”9 and that this is a “buyer-beware situation.”9
I understand that the compounds in PCDC are naturally occurring substances in our body. If it’s natural, why is it considered a drug?

Just because something is a naturally occurring substance does not mean that it is not a drug. Take insulin, adrenaline, human growth hormone, and erythropoietin, for example. They are natural substances in our body, all are considered drugs, and all are extremely dangerous at the wrong dose. The FDA considers something a drug if it affects the structure and function of the body. PCDC providers claim that it does just that.

What does FDA-Approval mean?

In the United States, prescription drugs are required to undergo rigorous laboratory, animal, and human clinical testing before they can be put on the market. The FDA reviews results of these studies to verify the identity, potency, purity, and stability of the ingredients as well to verify that the drug is safe and effective for its intended use. PCDC has not undergone any of the necessary testing required for FDA-approval. For more information on the drug approval process and the benefits of using drugs that have been FDA approved, please see the BOTOX®/Lipo-dissolve comparison page outlining the difference between an FDA-approved drug versus a non-FDA approved drug.

If PCDC is not approved, does that mean it’s being legally used off-label?

No. According to FDA, “off-label” use involves using an “approved” drug for an indication not in the approved labeling at the discretion of a physician10. Since PCDC is not approved, its use cannot be considered “off-label.” For more information, see Differences Between Lipo-dissolve and BOTOX® page.

Futhermore, the FDA has stated, “We are not aware of any phosphatidylcholine injectable products or sodium deoxycholate injectable products that could be used ‘off-label’ in ‘lipodissolve’ procedures.” Read more…

What data exists to demonstrate the safety and efficacy of phosphatidylcholine injections?

It is important to note that there have been numerous retrospective studies (i.e. historical observations) performed on the use of phosphatidylcholine injections for fat dissolution1,2and a few prospective non-placebo-controlled studies performed to test the efficacy of the procedure.11 However, to date there have been no prospective, placebo-controlled studies (those required for FDA approval) done on the use of PCDC for fat removal and therefore safety and efficacy cannot be confirmed. Placebo-controlled studies are those where participants are randomly assigned to receive either the placebo or the active substance. Neither the participant nor the doctor know which treatment the participant receives. The goal of this type of trial is to illustrate that it is the drug that is eliciting a response, not the placebo. With retrospective studies, one makes conclusions based on pre-existing data (i.e. you start with an answer and look backwards to selectively find data that supports your conclusion). Prospective trials, as required by the FDA, by their very structure prevent this from happening.


Aging is associated with reduced GH, IGF-I, and sex steroid axis activity and with increased abdominal fat. We employed a randomized, double-masked, placebo-controlled, noncross-over design to study the effects of 6 months of administration of GH alone (20 microg/kg BW), sex hormone alone (hormone replacement therapy in women, testosterone enanthate in men), or GH + sex hormone on total abdominal area, abdominal sc fat, and visceral fat in 110 healthy women (n = 46) and men (n = 64), 65-88 yr old (mean, 72 yr). GH administration increased IGF-I levels in women (P = 0.05) and men (P = 0.0001), with the increment in IGF-I levels being higher in men (P = 0.05). Sex steroid administration increased levels of estrogen and testosterone in women and men, respectively (P = 0.05). In women, neither GH, hormone replacement therapy, nor GH + hormone replacement therapy altered total abdominal area, sc fat, or visceral fat significantly. In contrast, in men, administration of GH and GH + testosterone enanthate decreased total abdominal area by 3.9% and 3.8%, respectively, within group and vs. placebo (P = 0.05). Within-group comparisons revealed that sc fat decreased by 10% (P = 0.01) after GH, and by 14% (P = 0.0005) after GH + testosterone enanthate. Compared with placebo, sc fat decreased by 14% (P = 0.05) after GH, by 7% (P = 0.05) after testosterone enanthate, and by 16% (P = 0.0005) after GH + testosterone enanthate. Compared with placebo, visceral fat did not decrease significantly after administration of GH, testosterone enanthate, or GH + testosterone enanthate. These data suggest that in healthy older individuals, GH and/or sex hormone administration elicits a sexually dimorphic response on sc abdominal fat. The generally proportionate reductions we observed in sc and visceral fat, after 6 months of GH administration in healthy aged men, contrast with the disproportionate reduction of visceral fat reported after a similar period of GH treatment of nonelderly GH deficient men and women. Whether longer term administration of GH or testosterone enanthate, alone or in combination, will reduce abdominal fat distribution-related cardiovascular risk in healthy older men remains to be elucidated.




Medical College, Jinhua College of Profession and Technology, Jinhua 321007, China.



To investigate the effects of Ginkgo biloba extract (GbE) on the glucose uptake rate and gene expression of glucose transporter 4 (GLUT4) in diaphragm of diabetic rats.


Forty SD male rats were randomly divided into normal control group (n=10) and model group (n=30). Diabetic models were induced by feeding with high-sucrose-high-fat diet and intraperitoneal injecting 25 mg X kg(-1) streptozotocin. 20 successful models were rearranged to two groups: diabetic group and GbE treatment group, 10 rats in each. Then the saline and 8 mg X kg(-1) x d(-1) of GbE were respectively intraperitoneal injected, once a day continuously for 8 weeks. The contents of fasting blood glucose (FBG), fasting insulin (FINS) were detected, respectively. The glucose uptake rate and gene expression of GLUT4 in diaphragm were determinated and the varieties of diaphragm ultrastructure were observed.


Compared with control group, levels of FBG and FINS obviously increased in diabetic rats (P < 0.01), but the glucose uptake rate and expression of GLUT4 mRNA in diaphragm decreased significantly (P < 0.05, P < 0.01). The ultrastructure in diabetic group under electron microscope indicated that diaphragm mitochondrion swelled and degenerated. The above changes were inhibited by GbE.


GbE can improve the glucose metabolism in diabetic rats and reduce the diabetes-induced diaphragm damage. The action mechanism of the drug may be related to promote the mRNA expression of GLUT4 in diaphragm and improve the uptake and metabolism of blood glucose.

[PubMed – indexed for MEDLINE]


Metabolic disorders, including type 2 diabetes and obesity, represent major health risks in industrialized countries. AMP-activated protein kinase (AMPK) has become the focus of a great deal of attention as a novel therapeutic target for the treatment of metabolic syndromes, because AMPK has been demonstrated to mediate, at least in part, the effects of a number of physiological and pharmacological factors that exert beneficial effects on these disorders. Thus, the identification of a compound that activates the AMPK pathway would contribute significantly to the treatment and management of such syndromes. In service of this goal, we have screened a variety of naturally occurring compounds and have identified one compound, cryptotanshinone, as a novel AMPK pathway activator. Cryptotanshinone was originally isolated from the dried roots of Salvia militorrhiza, an herb that is used extensively in Asian medicine and that is known to exert beneficial effects on the circulatory system. For the first time, in the present study, we have described the potent antidiabetic and antiobesity effects of cryptotanshinone, both in vitro and in vivo. Our findings suggest that the activation of the AMPK pathway might contribute to the development of novel therapeutic approaches for the treatment of metabolic disorders such as type 2 diabetes and obesity.

The number of Americans with type 2 diabetes is expected to increase by 50% in the next 25 years; hence, the prevention of type 2 diabetes is an important objective. Recent large-scale trials (the Diabetes Prevention Program and STOP-NIDDM) have demonstrated that therapeutic agents used to improve insulin sensitivity in diabetes, metformin and acarbose, may also delay or prevent the onset of type 2 diabetes in high-risk populations. Interestingly, an early report showed that vinegar attenuated the glucose and insulin responses to a sucrose or starch load (1). In the present report, we assessed the effectiveness of vinegar in reducing postprandial glycemia and insulinemia in subjects with varying degrees of insulin sensitivity.

Our study included nondiabetic subjects who were either insulin sensitive (control subjects, n = 8) or insulin resistant (n = 11) and 10 subjects with type 2 diabetes. Subjects provided written informed consent and were not taking diabetes medications. Fasting subjects were randomly assigned to consume the vinegar (20 g apple cider vinegar, 40 g water, and 1 tsp saccharine) or placebo drink and, after a 2-min delay, the test meal, which was composed of a white bagel, butter, and orange juice (87 g total carbohydrates). The cross-over trial was conducted 1 week later. Blood samples were collected at fasting and 30 and 60 min postmeal for glucose and insulin analyses. Whole-body insulin sensitivity during the 60-min postmeal interval was estimated using a composite score (2).

Fasting glucose concentrations were elevated ∼55% in subjects with diabetes compared with the other subject groups (P < 0.01, Tukey’s post hoc test), and fasting insulin concentrations were elevated 95–115% in subjects with insulin resistance or type 2 diabetes compared with control subjects (P < 0.01). Compared with placebo, vinegar ingestion raised whole-body insulin sensitivity during the 60-min postmeal interval in insulin-resistant subjects (34%, P = 0.01, paired t test) and slightly improved this parameter in subjects with type 2 diabetes (19%, P = 0.07). Postprandial fluxes in insulin were significantly reduced by vinegar in control subjects, and postprandial fluxes in both glucose and insulin were significantly reduced in insulin-resistant subjects (Fig. 1).

These data indicate that vinegar can significantly improve postprandial insulin sensitivity in insulin-resistant subjects. Acetic acid has been shown to suppress disaccharidase activity (3) and to raise glucose-6-phosphate concentrations in skeletal muscle (4); thus, vinegar may possess physiological effects similar to acarbose or metformin. Further investigations to examine the efficacy of vinegar as an antidiabetic therapy are warranted.

Figure 1—

View larger version:

Figure 1—

Effects of vinegar (□) and placebo (⧫) on plasma glucose (AC) and insulin (DF) responses after a standard meal in control subjects, insulin-resistant subjects, and subjects with type 2 diabetes. Values are means ± SE. The P values represent a significant effect of treatment (multivariate ANOVA repeated-measures test).



  1. Ebihara K, Nakajima A: Effect of acetic acid and vinegar on blood glucose and insulin responses to orally administered sucrose and starch. Agric Biol Chem 52:1311–1312, 1988
  2. Matsuda M, DeFronzo RA: Insulin sensitivity indices obtained from oral glucose tolerance testing. Diabetes Care 22:1462–1470, 1999
  3. Ogawa N, Satsu H, Watanabe H, Fukaya M, Tsukamoto Y, Miyamoto Y, Shimizu M: Acetic acid suppresses the increase in disaccharidase activity that occurs during culture of Caco-2 cells. J Nutr 130:507–513, 2000
  4. Fushimi T, Tayama K, Fukaya M, Kitakoshi K, Nakai N, Tsukamoto Y, Sato Y: Acetic acid feeding enhances glycogen repletion in liver and skeletal muscle of rats. J Nutr 131:1973–1977, 2001


BALTIMORE– Two studies presented at the American College of Sports Medicine’s 57thBaltimore show that chocolate milk may be a worthwhile post-exercise recovery beverage. Annual Meeting in

William Lunn, Ph.D., who collaborated on both research studies conducted in the lab of Nancy Rodriguez, Ph.D., FACSM, found in the first study that ingesting chocolate milk after a run supported skeletal muscle protein synthesis during recovery.

Eight male runners in relatively good training shape completed two runs (each 45 minutes at 65 percent of their maximum levels) during two weeks of eating a balanced diet matched to their individual caloric needs. Following each run, the study participants drank either 16 ounces of fat-free chocolate milk or 16 ounces of a carbohydrate-only beverage, matched for calories with the milk.

Following muscle biopsy samples taken during a three-hour recovery period after each run, Lunn found that runners who drank fat-free chocolate milk during recovery had heightened markers of muscle protein repair compared to the carbohydrate drink.

“It’s always helpful for exercisers to learn of additional options for recovery drinks,” Lunn said. “Chocolate milk can be relatively inexpensive compared to commercially available recovery drinks and is easy to make at home, making it a viable and palatable option for many people.”

The second study showed that chocolate milk also contributes to replenishing glycogen stores in muscles, a source of fuel during prolonged exercise. Muscle glycogen levels in the same eight male runners were tested 30 minutes and 60 minutes following ingestion of either the fat-free chocolate milk or the carbohydrate beverage.

Muscle glycogen content was greater for the chocolate milk drinkers at both measurement times, further supporting the use of this drink in recovery nutrition strategies.

The American College of Sports Medicine is the largest sports medicine and exercise science organization in the world. More than 35,000 international, national and regional members and certified professionals are dedicated to advancing and integrating scientific research to provide educational and practical applications of exercise science and sports medicine.


Note: These studies were supported by a grant from the National Dairy Council and National Fluid Milk Processor Promotion Board.

The conclusions outlined in this news release are those of the researchers only, and should not be construed as an official statement of the American College of Sports Medicine.