Аферы Подделки Криминал // Aferizm.ru

Есть предложение резко завязать с оффтопиком в рассылке, посвящённой
новостям науки.
Игорь.

4 января 2009 г. 17:45 пользователь Stas AV <stas_***@m*****.ru> написал:

--
Дискуссионный лист сайта Bessmertie.Ru

Original Message From: "Igor Artyuhov" <artyuh***@m*****.ru>

Исправляемся :-)

Irvingia gabonensis. Ирвингия габонская, или дика, удика, меба, муба
(Конго), ботуба, эту (Камерун)

В статье описано, что компоненты экстракта этого растения радикально
изменяют метаолический синдром, и стойкость ожирения.
Радикально ( по нескольким механизмам)
Исследователи сами удивляются, похоже это самое лучшее средство для решения
проблемы избыточного веса, метаболического синдрома из всех известных на
сегодня.
More Weight Loss than Any Other Discovery in Supplement History
By William Faloon

I'll never forget an experience I had at a medical conference 14 years ago.
A renowned scientist persistently asked me to sell him the hormone leptin.
When given to obese mice, leptin caused weight loss of 40% after 33 days.
In human terms, that equates to a 250-pound person shrinking to 150 pounds
in a short time. The problem was that leptin did not work in humans, if they
were not leptin-deficient to begin with.1
This obese scientist kept badgering me because he thought I knew how to get
leptin. When I repeatedly said it would not work for him, he asked me why it
would not work. Back in 1994, I did not know that answer.
In a breakthrough that may reverse today's epidemic of obesity, a natural
compound has been discovered that circumvents the molecular factors involved
in obesity ... including a phenomenon known as ``leptin-resistance.''2-4 This
means that for the first time, humans can benefit from their own leptin
because it can now enter cells and do what it did for obese mice ... induce
massive weight loss!
In a recent controlled study, humans taking this new compound lost 28 pounds
over a 10-week period compared to less than 3 pounds in the placebo group.5
Unlike other weight loss studies that mandate at least some moderation in
food intake, these study participants did not alter their diet in any way.
Equally remarkable are results showing the same mechanisms that enable this
compound to remove body fat also lower heart attack risk factors like
LDL,5,6 glucose7,8 and C-reactive protein.5
In this article, I will discuss scientific findings showing how this new
compound produces more impressive weight loss results than any other drug,
nutrient or hormone in medical history.
Scientists have identified specific factors that cause aging people to
accumulate unwanted fat pounds. The problem has been that up until now,
there has not been an effective way to circumvent these underlying causes of
today's obesity epidemic.
The corpulent mass that accrues on our aging bodies can be compared to the
growth of malignant tumors. This analogy goes beyond ever-increasing fat
bulges and extends to how fat cells resist eradication. Like cancer, fat
cells deploy multiple survival mechanisms when their existence is
threatened.
So while many ways have been developed to assist people in losing weight,
nothing has been shown to circumvent the natural ability of adipocytes (fat
cells) to propagate and retain excess fat ... until now!
OBESITY IS CAUSED BY:
Imbalance between energy (food) intake and energy expenditure
Hormone imbalance
Genetic factors
Multiple physiological and molecular mechanisms influencing body fat
regulation.
It is obesity cause number four above that is the most prevalent factor
involved in age-associated weight gain. Fortunately, it is now possible to
control these obesity-inducing mechanisms using a natural plant extract.

How fat cells accumulate fat
Adipocytes (fat cells) function to store calories in the body. When energy
is needed, specific command signals mobilize adipocytes to release their
stored fat.
The adipocyte is the primary site for fat storage. Under the microscope,
adipocytes appear bloated with triglycerides, which is the form that most
fat exists in the body.9-10
Age-related weight gain occurs when adipocytes (fat cells) accumulate a
large amount of triglycerides and become enlarged. Obesity is characterized
at the cellular level by an increase in the number and size of adipocytes in
fat tissue.11-12
Adipocytes accumulate excess triglycerides due to overeating, insufficient
physical activity, hormone imbalance and other causes. These factors,
however, fail to address the reason why aging individuals seem to put on fat
pounds despite making great efforts to eat less, taking dietary supplements
and following other practices that should in theory lead to weight loss.
Role of command signals in regulating adipocytes
Young, physically active people can consume lots of calories, often without
becoming overweight. One might wonder what mechanism besides physical
activity enables these healthy young bodies to limit the amount of ingested
fat stored in their adipocytes.
The answer is the adipocyte command signal network that controls the storage
and release of triglycerides from fat cells. These signals also regulate
adipocyte proliferation.
The aging process adversely affects the adipocyte command signal network,
which helps explain the difficulty maturing individuals have in controlling
their weight.
The three critical adipocyte command signals
Adipocytes regulate their size and number by secreting command signals.13
One such signal is the hormone leptin, which is derived from the Greek term
leptos, meaning thin.
Leptin is released by adipocytes to perform two critical functions. First it
signals the brain that enough food has been ingested and shuts down
appetite.13-19 It then seems to exert a process whereby triglycerides stored
in adipocytes are broken down into fatty acids that can be used in energy
production.20-22
The second command signal released by adipocytes is a hormone called
adiponectin. This hormone is an important modulator of insulin sensitivity.
Adiponectin has been shown to have anti-atherosclerotic, anti-inflammatory
and anti-diabetic roles.23-28 High circulating levels of adiponectin have
been shown to protect against coronary artery disease, whereas low
adiponectin levels are observed in overweight individuals.25, 26, 29-32 The
insulin-sensitizing effects of adiponectin represent a novel treatment
target for insulin resistance, Type 2 diabetes, and obesity.26, 28-41
The third adipocyte command signal is glycerol-3-phosphate dehydrogenase.
This enzyme is produced in adipocytes to help convert blood sugar into
triglyceride stores in fat cells.42
The three adipocyte command signals are thus:
Leptin
Adiponectin
Glycerol-3-phosphate dehydrogenase
An ideal weight loss agent would increase adiponectin, decrease
glycerol-3-phosphate dehydrogenase and inhibit barriers in the aging body
that block the utilization of leptin.
Discovery of a West African medicinal food
Medical discoveries often start with accidental observations. For instance,
British sailors where encouraged to eat limes to prevent scurvy long before
anyone even knew about vitamin C. Scurvy is the acute disease one contracts
when vitamin C intake is deficient.
Anecdotal information indicated that a West African medicinal food called
Irvingia gabonensis might produce some weight loss effects. A scientific
analysis of various Irvingia extracts revealed that they produced a wide
range of biological properties that would not only induce weight loss, but
also reduce the most common risk factors involved in atherosclerosis and
type 2 diabetes.5-7, 43, 46, 51, 52, 54
Small studies were conducted to identify which Irvingia extract worked best
in humans. Findings from the first placebo-controlled human study showed the
Irvingia extract selected caused fat loss and also markedly reduced total
cholesterol (by 39%), LDL (by 45%), glucose (by 32%), and triglycerides (by
45%).6
How Irvingia extract works
Weight loss-inducing agents, be they supplements, hormones or drugs,
typically function via only one mechanism. Unfortunately, adipocytes possess
numerous routes to ensure their continued growth and proliferation. These
survival characteristics of adipocytes explain why logical methods to
promote weight loss have produced only mediocre results.
Amylase is an enzyme that converts starch to sugar in the digestive tract.
There is an FDA-approved weight loss drug called Acarbose(R) that inhibits
amylase and thereby reduces the amount of sugar absorbed into the
bloodstream. White kidney bean extract does the same thing.44,46 Only
moderate weight loss benefits, however, have been shown with amylase
inhibitors. Irvingia is an amylase inhibitor, but this is not its primary
mechanism of fat loss induction.6, 46
Adiponectin is a hormone that plays a critical role in metabolic
abnormalities that are associated with Type 2 diabetes, obesity, and
atherosclerosis.33, 26, 28, 34-41 Higher levels of adiponectin enhance
insulin sensitivity, and enhancing insulin sensitivity is important to
long-term metabolic health as we age. Adipogenic transcriptional factors
involved with adiponectin are also involved in the formation of new
adipocytes, fat burning and endothelial function.47-49 Irvingia increases
beneficial adiponectin levels and inhibits adipocyte differentiation
mediated through the suppression of adipogenic transcription factors.49

Click to enlarge
Glycerol-3-phosphate dehydrogenase is an enzyme that facilitates the
conversion of blood glucose into triglycerides that increase adipocyte size.
Elevated glycerol-3-phosphate dehydrogenase might contribute to the increase
of triacylglycerol synthesis in obese subjects.56 Irvingia inhibits
glycerol-3-phosphate dehydrogenase, thus reducing the amount of ingested
sugars that are converted to body fat.42
Leptin is a hormone secreted from adipocytes. Leptin is much more abundant
in the blood of obese individuals. This may at first seem illogical since
leptin functions to turn off appetite while promoting breakdown of
triglycerides that bloat adipocytes. One reason obese people have higher
blood levels of leptin is that C-reactive protein binds with leptin and
impairs leptin transport across the blood-brain-barrier and leptin signaling
at a cellular level.50
The release of C-reactive protein by adipocytes, a leptin-binding protein,
neutralizes the natural adipocyte-controlling effects of leptin. Obese
people have more adipocytes that secrete leptin and C-reactive protein.17,
50, 51 The result is that more leptin accumulates in the blood of obese
individuals because it is not able to be picked up by leptin receptor sites
on cell membranes.57 Irvingia is associated with dramatically lower levels
of C-reactive protein, thereby unblocking the ``leptin resistance'' that
causes so many weight loss programs to fail.5
Irvingia may induce fat-loss via four different mechanisms:
It up-regulates the expression of adiponectin, thereby improving insulin
sensitivity.
It is associated with lower levels of C-reactive protein and helps restore
the dual weight control effects of leptin.
It inhibits glycerol-3-phosphate dehydrogenase, thereby reducing fatty acid
formation in the body and inhibiting the amount of blood glucose that
converts to fat.
It inhibits the enzyme amylase, thus reducing the amount of ingested
starches that will be absorbed as sugar.

Effect of Irvingia on weight loss, blood fats and glucose
In 1990, researchers studied the effects of Irvingia on eleven human Type 2
diabetics. Compared to baseline, there were significant reductions in blood
triglyceride levels (16%), total cholesterol (30%), LDL (39 %), and glucose
(38%), while HDL-cholesterol levels were increased by 29% after four-week
supplementation. These desirable biochemical effects were accompanied by
improved clinical states.43
In 2005, researchers fed guinea pigs a high-fat diet with or without
Irvingia. The guinea pigs receiving the Irvingia displayed a significant
increase in beneficial HDL accompanied by a significant decrease in
triglycerides and LDL. After three weeks, the Irvingia-supplemented animals
lost more than 7% of their body weight; whereas the control group fed the
same high-fat diet (without Irvingia) showed more than 8% increase in body
weight.52

In 2006, researchers studied the effect of Irvingia in rats who were
artificially induced to develop diabetes. Just a single oral dose of
Irvingia lowered plasma glucose two hours after treatment.46
Another study in 2006 evaluated the effects of Irvingia in slowing the
intestinal absorption of glucose in healthy rats. The results showed a
significant reduction in after-meal glucose blood level and lower subsequent
fasting glucose scores.54
The first double-blind study in humans occurred in 2005. Twenty eight of the
subjects received Irvingia while twelve were given a placebo. All subjects
maintained their normal calorie intake. After 30 days, subjects taking
Irvingia lost 12.3 pounds. The Irvingia group also experienced significant
reductions in total cholesterol, LDL, triglycerides and an increase in HDL.6
The most significant Irvingia study

Based on consistent findings showing multiple beneficial effects of
Irvingia, a larger study was conducted on overweight and obese participants
over a 10-week period. Participants were randomly divided in two groups, one
that received Irvingia extract (150 mg twice daily), and the other was given
a placebo, while maintaining the same diet and amount of physical exercise.5
Body weight and the following blood levels were measured at baseline:
Total Cholesterol, LDL and HDL
Fasting glucose
Leptin
Adiponectin
C-reactive protein
The chart below shows the weight loss effects measured at three different
times during the ten week study:5
Baseline weight4 weeks8 weeks10 weeks
Irvingia group215 pounds207 pounds197 pounds187 pounds
Placebo group212 pounds210 pounds209 pounds211 pounds

The chart above shows the Irvingia group lost 28 pounds, whereas the placebo
group lost virtually no weight.
The results from the blood measurements showed equally remarkable effects
after ten weeks as follows:5
GlucoseCholesterolLDLCRP*AdiponectinLeptin
Irvingia group-22%-26%-27%-52%+160%-49%**
Placebo group-5.2%-1.9%-4.8%-1%+23%-9%
*C-reactive protein
**Reduced blood levels of leptin indicate it is binding to leptin receptor
sites on cells and performing its weight control function. Higher leptin
blood levels indicate "leptin-resistance," just as higher blood insulin
levels indicate "insulin resistance."

These remarkable blood marker changes reveal specific mechanisms responsible
for the profound weight loss effects observed in subjects receiving
Irvingia. These beneficial blood marker changes would also confer
considerable protection against diabetes and vascular disease beyond the fat
loss benefits.
When assessing body composition in these study subjects, the following
changes were measured at 10 weeks:5
Waist ReductionFat Loss
Irvingia group16.2%18.4%
Placebo group5.0%5.7%

This historic study demonstrated that Irvingia induced more weight loss in a
shorter period of time than any other compound ever tested. Participants who
received Irvingia had significant improvements in body composition and
reductions in blood measurements of cardiovascular and diabetes risk.
The charts below show the percentage of changes seen in the Irvingia group
compared to the placebo group.

Irvingia on Weight & Fasting Blood GlucoseIrvingia on Total Cholesterol &
LDL Cholesterol

Irvingia on C-reactive Protein & AdiponectinIrvingia on Leptin

Dosage
Scientists have spent many years identifying the specific Irvingia extract
that promotes the greatest amount of weight loss, while reducing blood fat
(lipid) and glucose levels.
In the most significant study to date, it required only 150 mg of
standardized Irvingia extract taken two times a day to produce the dramatic
results, i.e. 28 pounds of weight loss in subjects taking Irvingia extract
compared to less than 3 pounds of weight loss in the placebo group.
Considering the profound effect of Irvingia in sharply reducing blood
glucose and cholesterol, the dose of 150 mg of Irvingia taken two times a
day should not be exceeded.
Precautions
Optimal cholesterol levels range from 180 to 200 mg/dL. Cholesterol over 200
increases heart attack risk, whereas cholesterol below 150-160 mg/dL seems
to increase overall mortality, probably from diseases like hemorrhagic
stroke and cancer along with deficiencies of hormones that are made from
cholesterol.
If you use cholesterol-lowering drugs and start taking Irvingia, have your
blood tested after 30 days to make sure that your cholesterol level is not
being lowered too much. If your total cholesterol drops below 160, ask your
doctor to consider reducing the dose or eliminating your statin drug.
Hypoglycemics (low blood sugar) should use this product with caution as it
can significantly lower blood glucose levels.
Diabetics taking medications to lower glucose levels should use this product
with caution as it might cause glucose to drop too low. Diabetics are
encouraged to carefully monitor their blood glucose levels, in coordination
with their physician, to make sure the proper doses of anti-diabetic drug(s)
are taken. If blood glucose levels drop too low, ask your doctor if the dose
of anti-diabetic drug can be lowered, or the drug(s) discontinued
altogether. If a diabetic experiences significant weight loss with Irvingia,
their need for anti-diabetic drugs may be reduced or eliminated. Careful
self measurement of blood glucose levels is crucial for all diabetics.
IRVINGIA
has been shown to work via multiple pathways to promote effective fat loss
by such mechanisms as:
Inhibiting ?-amylase activity, reducing the absorption of sugar
Reducing glucose levels and insulin induced lipogenesis
Reducing adipocyte triglycerides and the glucose-3-phophate dehydrogenase
enzyme (thus inhibiting the conversion of glycerol to triglycerides)
Reducing immune mediated inflammatory-molecule (CRP) binding to leptin,
thereby reducing leptin resistance
Lowering serum leptin levels
Increasing adiponectin levels (anti-atherogenic, anti-inflammatory and
anti-diabetic effects)
Reducing PPARgamma expression, which has been implicated in insulin
resistance and the pathology of numerous diseases including obesity,
diabetes, atherosclerosis and cancer

Summary and warning to not overeat
Endeavors to manage age-associated surplus body fat buildup have been
challenging.
Just when new methods are discovered to reduce fat stores, scientists
uncover additional mechanisms by which adipocytes retain excess
triglycerides.
Irvingia seems to overcome the multiple escape routes that enable fat cells
(adipocytes) in aging bodies to resist eradication.
Last year I wrote an article titled ``Why a 100% Effective Diet Pill Would
Lead to a Health Catastrophe.''55 My article stated that most people restrict
their calorie intake not for health reasons but to avoid becoming too fat. I
warned that if a diet pill ever emerged that did not require food
restriction, most people would overeat themselves into an early grave.
It is still too early to know for sure if Irvingia will prove to be a 100%
effective diet pill.
With our knowledge about the health and longevity benefits of restricting
calorie intake, I beg, plead, and reiterate my point that if you find an
effective method to lose weight without dieting, please continue to control
calorie intake anyway in order to extend your life.

In other words, if Irvingia were to work for you as well as it did for the
study subjects, please do not overeat, as excess calorie intake is a leading
cause of cancer, vascular disease, and accelerated aging. The good news is
that by freeing up leptin to bind to hunger-control centers in the brain,
most people will find their appetite is reduced when taking Irvingia, thus
eabling them to effortlessly ingest fewer calories.
Note: The issue of Life Extension Magazine that members will receive in
early January 2009 will feature an in-depth scientific report on obesity and
the role that adipocyte modulating agents like leptin and adiponectin play
in regulating body fat storage.
References
1. Zelissen PM, Stenlof K, Lean ME, et al. Effect of three treatment
schedules of recombinant methionyl human leptin on body weight in obese
adults: a randomized, placebo-controlled trial. Diabetes Obes Metab. 2005
Nov; 7(6):755-61.
2 Patel SB, Reams GP, Spear RM, Freeman RH, Villarreal D. Leptin: linking
obesity, the metabolic syndrome, and cardiovascular disease. Curr Hypertens
Rep. 2008 Apr;10(2):131-7.
3. Scarpace PJ, Zhang Y. Elevated leptin: consequence or cause of obesity?
Front Biosci. 2007 May 1;12:3531-44. Review.
4. Enriori PJ, Evans AE, Sinnayah P, Cowley MA. Leptin resistance and
obesity. Obesity. 2006 Aug;14 Suppl 5:254S-258S. Review.
5. Ngondi JL, Matsinkou R, Oben JE. The use of Irvingia gabonensis extract
(IGOB131) in the management of metabolic syndrome in Cameroon. Nutrition J.
2008 (submitted).
6. Ngondi JL, Oben JE, Minka SR. The effect of Irvingia gabonensis seeds on
body weight and blood lipids of obese subjects in Cameroon. Lipids Health
Dis. 2005 May 25;4:12.
7. Omoruyi F, Adamson I. Digestive and hepatic enzymes in
streptozotocin-induced diabetic rats fed supplements of dikanut (Irvingia
gabonensis) and cellulose. Ann Nutr Metab. 1993 37(1):14-23.
8. Adamson I, Okafor C, Abu-Bakare A. A supplement of Dikanut (Irvingia
gabonesis) improves treatment of type II diabetics. West Afr J Med. 1990
Apr-Jun;9(2):108-15.
9. Smith J, Al-Amri M, Dorairaj P, Sniderman A. The adipocyte life cycle
hypothesis. Clin Sci (Lond). 2006 Jan;110(1):1-9.
10. Azain MJ. Role of fatty acids in adipocyte growth and development. J
Anim Sci. 2004 Mar;82(3):916-24.
11. Kiess W, Petzold S, To:pfer M, Garten A, Blu:her S, Kapellen T, Ko:rner A,
Kratzsch J. Adipocytes and adipose tissue.Best Pract Res Clin Endocrinol
Metab. 2008 Feb;22(1):135-53.
12. Rabkin SW. Epicardial fat: properties, function and relationship to
obesity.Obes Rev. 2007 May;8(3):253-61.
13. Ahima RS, Lazar MA. Adipokines and the peripheral and neural control of
energy balance. Mol Endocrinol. 2008 May;22(5):1023-31.
14. Friedman JM. The function of leptin in nutrition, weight, and
physiology. Nutr Rev. 2002 Oct;60(10 Pt 2):S1-14.
15. Cohen P, Zhao C, Cai X, et al. Selective deletion of leptin receptor in
neurons leads to obesity. J Clin Invest. 2001 Oct;108(8):1113-21.
16. Campfield LA, Smith FJ, Guisez Y, Devos R, Burn P. Recombinant mouse OB
protein: evidence for a peripheral signal linking adiposity and central
neural networks. Science. 1995 Jul 28;269(5223):546-9.
17. Bray GA, York DA. Leptin and clinical medicine: a new piece in the
puzzle of obesity. J Clin Endocrinol Metab. 1997 Sep;82(9):2771-6.
18. Maffei M, Halaas J, Ravussin E, et al. Leptin levels in human and
rodent: measurement of plasma leptin and ob RNA in obese and weight-reduced
subjects. Nat Med. 1995 Nov;1(11):1155-61.
19. Qi Y, Takahashi N, Hileman SM, et al. Adiponectin acts in the brain to
decrease body weight. Nat Med. 2004 May;10(5):524-9.
20. Kim WK, Lee CY, Kang MS, et al. Effects of Leptin on Lipid Metabolism
and Gene Expression of Differentiation-Associated Growth Factors and
Transcription Factors during Differentiation and Maturation of 3T3-L1
Preadipocytes. Endocr J. 2008 May 23. [Epub ahead of print]
21. Tajima D, Masaki T, Hidaka S, Kakuma T, Sakata T, Yoshimatsu H. Acute
central infusion of leptin modulates fatty acid mobilization by affecting
lipolysis and mRNA expression for uncoupling proteins. Exp Biol Med
(Maywood). 2005 Mar;230(3):200-6.
22. Fru:hbeck G, Go'mez-Ambrosi J, Salvador J. Leptin-induced lipolysis
opposes the tonic inhibition of endogenous adenosine in white adipocytes.
FASEB J. 2001 Feb;15(2):333-40.
23. Pajvani UB, Du X, Combs TP, et al. Structure-function studies of the
adipocyte-secreted hormone Acrp30/adiponectin. Implications for metabolic
regulation and bioactivity. J Biol Chem. 2003 Mar 14;278(11):9073-85.
24. Matsuzawa Y. Adiponectin: Identification, physiology and clinical
relevance in metabolic and vascular disease. Atheroscler Suppl. 2005
May;6(2):7-14.
25. Okui H, Hamasaki S, Ishida S, et al. Adiponectin is a better predictor
of endothelial function of the coronary artery than HOMA-R, body mass index,
immunoreactive insulin, or triglycerides. Int J Cardiol. 2008 May
7;126(1):53-61.
26. Fasshauer M, Paschke R, Stumvoll M. Adiponectin, obesity, and
cardiovascular disease. Biochimie. 2004 Nov;86(11):779-84.
27. Gil-Campos M, Can~ete RR, Gil A. Adiponectin, the missing link in insulin
resistance and obesity. Clin Nutr. 2004 Oct;23(5):963-74.
28. Shand BI, Scott RS, Elder PA, George PM. Plasma adiponectin in
overweight, nondiabetic individuals with or without insulin resistance.
Diabetes Obes Metab. 2003 Sep;5(5):349-53.
29. Nakamura T, Kodama Y, Takano H, et al. Increase in circulating levels of
adiponectin after treatment with statin and fibrate in patients with
coronary artery disease and hyperlipidemia. Atherosclerosis. 2007
Aug;193(2):449-51.
30. Pischon T, Girman CJ, Hotamisligil GS, Rifai N, Hu FB, Rimm EB. Plasma
adiponectin levels and risk of myocardial infarction in men. JAMA. 2004 Jul
7;292(1):40.
31. Han SH, Quon MJ, Kim JA, Koh KK. Adiponectin and cardiovascular disease:
response to therapeutic interventions. J Am Coll Cardiol. 2007 Feb
6;49(5):531-8.
32. Kumada M, Kihara S, Sumitsuji S, et al. Association of
hypoadiponectinemia with coronary artery disease in men. Arterioscler Thromb
Vasc Biol. 2003 Jan 1;23(1):85-9.
33. Berger J, Moller DE. The mechanisms of action of PPARs. Annu Rev Med.
2002 53:409-435.
34. Yamauchi T, Kamon J, Waki H, et al. The fat-derived hormone adiponectin
reverses insulin resistance associated with both lipoatrophy and obesity.
Nat Med. 2001 7:941-946.
35. Kadowaki T, Yamauchi T. Adiponectin and adiponectin receptors. Endocr
Rev. 2005 May;26(3):439-51.
36. Kershaw EE, Flier JS. Adipose tissue as an endocrine organ. J Clin
Endocrinol Metab. 2004 Jun;89(6):2548-56.
37. Hotta K, Funahashi T, Bodkin NL, et al. Circulating concentrations of
the adipocyte protein adiponectin are decreased in parallel with reduced
insulin sensitivity during the progression to type 2 diabetes in rhesus
monkeys. Diabetes. 2001 May;50(5):1126-33.
38. Arita Y, Kihara S, Ouchi N, et al. Paradoxical decrease of an
adipose-specific protein, adiponectin, in obesity. Biochem Biophys Res
Commun. 1999 Apr 2;257(1):79-83.
39. Ryo M, Nakamura T, Kihara S, et al. Adiponectin as a biomarker of the
metabolic syndrome. Circ J. 2004 Nov;68(11):975-81.
40. Yatagai T, Nagasaka S, Taniguchi A, et al. Hypoadiponectinemia is
associated with visceral fat accumulation and insulin resistance in Japanese
men with type 2 diabetes mellitus. Metabolism. 2003 Oct;52(10):1274-8.
41. Yamamoto Y, Hirose H, Saito I, Nishikai K, Saruta T. Adiponectin, an
adipocyte-derived protein, predicts future insulin resistance: two-year
follow-up study in Japanese population. J Clin Endocrinol Metab. 2004
Jan;89(1):87-90.
42. Wise LS, Green H. Participation of one isozyme of cytosolic
glycerophosphate dehydrogenase in the adipose conversion of 3T3 cells. J
Biol Chem. 1979 Jan 25;254(2):273-5.
43. Adamson I, Okafor C, Abu-Bakare A. A supplement of Dikanut (Irvingia
gabonesis) improves treatment of type II diabetics. West Afr J Med. 1990
Apr-Jun;9(2):108-15.
44. Udani J, Hardy M, Madsen DC. Blocking carbohydrate absorption and weight
loss: a clinical trial using Phase 2 brand proprietary fractionated white
bean extract. Altern Med Rev. 2004 Mar;9(1):63-9.
45. Celleno L, Tolaini MV, D'Amore A, Perricone NV, Preuss HG. A dietary
supplement containing standardized Phaseolus vulgaris extract influences
body composition of overweight men and women. Int J Med Sci. 2007 Jan
24;4(1):45-52.
46. Ngondi JL, Djiotsa EJ, Fossouo Z, Oben J. Hypoglycaemic effect of the
methanol extract of irvingia gabonensis seeds on streptozotocin diabetic
rats. Afr J Trad CAM. 2006 3:74-7.
47. Rosen ED, Walkey CJ, Puigserver P, Spiegelman BM. Transcriptional
regulation of adipogenesis. Genes Dev. 2000 Jun 1;14(11):1293-307.
48. Gustafson B, Jack MM, Cushman SW, Smith U. Adiponectin gene activation
by thiazolidinediones requires PPAR gamma 2, but not C/EBP alpha-evidence
for differential regulation of the aP2 and adiponectin genes. Biochem
Biophys Res Commun. 2003 Sep 5;308(4):933-9.
49. Oben JE, Blum K. Inhibition of OB131 Irvingia gabonensis seed extract
(gabonectin(tm)) on adipogenesis as mediated via down regulation of the PPAR?
and leptin genes and up-regulation of the adiponectin gene. Lipids Health
Dis. 2008. (submitted)
50. Sinha MK, Opentanova I, Ohannesian JP, et al. Evidence of free and bound
leptin in human circulation. Studies in lean and obese subjects and during
short-term fasting. J Clin Invest. 1996 Sep 15;98(6):1277-82.
51. Dagogo-Jack S, Fanelli C, Paramore D, Brothers J, Landt M. Plasma leptin
and insulin relationships in obese and nonobese humans. Diabetes. 1996
May;45(5):695-8.
52. Ngondi JL, Makamto SC, Oben J. Irvingia gabonensis on body weight and
bloods lipids in normolipidemic guinea pigs. J Food Technology. 2005;3(4):
472-474.
53. Available at: http://www.bioline.org.br/request?tc06054. Accessed: Sept.
10, 2008.
54. Ngondi JL, Fossouo E, Djiotsa EJ, Oben J. Glycaemic variations after
administration of Irvingia gabonensis seeds fractions in normoglycemic rats.
Afr J Trad CAM. 2006;3:94-101.
55. Available at:
http://www.lef.org/magazine/mag2008/mar2008_Why-an-Effective-Diet-Pill-Would-Lead-to-a-Health-Catastrophe_01.htm.
Accessed: Sept. 10, 2008.
56. Swierczynski J, Zabrocka L, Goyke E, Raczynska S, Adamonis W, Sledzinski
Z. Enhanced glycerol 3-phosphate dehydrogenase activity in adipose tissue of
obese humans. Mol Cell Biochem. 2003 Dec;254(1-2):55-9.
57. Chen K, Li F, Li J, et al. Induction of leptin resistance through direct
interaction of C-reactive protein with leptin. Nat Med. 2006
Apr;12(4):425-32

http://www.lef.org/magazine/mag2008/ss2008_report_more-weight-loss.htm

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Дискуссионный лист сайта Bessmertie.Ru

Спасибо, Игорь!
Ценная информация, я об этом не знал.
Irvingia gabonensis - родственница манго, которое широко применяется в
Тибетской Медицине.
Genetic variation was assessed in the two bush mango species, Irvingia
gabonensis and I. wombolu, valuable multipurpose fruit trees from central
and west Africa that are currently undergoing domestication. A total of 130
individuals sampled from Cameroon, Nigeria and Gabon were analysed using 74
random amplified polymorphic DNAs (RAPDs). Significant genetic integrity was
found in the two morphologically similar species (among-species analysis of
molecular variance [AMOVA] variance component 25.8%, P < 0.001), with no
evidence of hybridization, even between individuals from areas of sympatry
where hybridization was considered probable. Results suggest that
large-scale transplantation of either species into new habitats will
probably not lead to genetic introgression from or into the other species.
Therefore, subsequent cultivation of the two species should not be hindered
by this consideration, although further studies on the potential for
hybridization/introgression between these species would be prudent.
Significant genetic differentiation of both species (among-countries within
species, nested AMOVA variance component 9.8%, P < 0.001) was observed over
the sampled regions, and genetic similarity of samples decreased
significantly with increasing geographical distance, according to number of
alleles in common (NAC) analysis. 'Hot spots' of genetic diversity were
found clustered in southern Nigeria and southern Cameroon for I. wombolu,
and in southern Nigeria, southern Cameroon and central Gabon for I.
gabonensis. The possible reasons for this distribution of genetic variation
are discussed, but it may reflect evolutionary history, as these populations
occur in areas of postulated Pleistocene refugia. The application of these
results to domestication programmes and, in the light of extensive
deforestation in the region, conservation approaches, is discussed.

http://www.ncbi.nlm.nih.gov/pubmed/10886647?ordinalpos=14&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum

Нужно будет более пристально приглядеться к манго, который более доступен.

С уважением, Вадим Асадулин.

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Дискуссионный лист сайта Bessmertie.Ru

Original Message From: "Igor Artyuhov" <artyuh***@m*****.ru>

Дискуссионный лист сайта Bessmertie.Ru
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