Hoodia gordonii

Hoodia gordonii is a small shrub (falsely said to be a cactus) that is claimed to suppress appetite. It seems the main bioactive (P57) cannot easily reach the brain to do this, and aside from failures of hoodia to suppress the appetite it may also be mildly toxic and imprudent to supplement.

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Hoodia gordonii is a small plant that is used as a famine food (to suppress appetite and thirst, to make suffering a famine a bit more bearable) and due to that is sought after for possible appetite suppressive effects. The first introduction of Hoodia to the first world (Europe and North America) was based on preliminary studies associated with the company producing Hoodia, and the lone independent study on Hoodia has noted that active dose recommended for a supplement not only failed to reduce appetite but was also associated with some mild and irregular toxic effects that need to be further investigated.

This plant appears to be a source of a large amount (well over 30) steroidal glycosides, and only one is said to be the activ ingredient (P57) yet most of the steroidal glycosides have no research on them. Due to this, the possible toxic effects in humans (confirmed in mice), and both the inefficacy on reducing appetite while having no other apparent marketable effects Hoodia gordonii does not appear to hold any promise for a dietary supplement.

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Also Known As

Hoodia, Veldkos, Slimming cactus, Trichocaulon gordonii, Stapelia gordonii


Do Not Confuse With

Garcinia cambogia (another ineffective appetite suppressant)


Things to Note

  • Possible CYP3A4 inhibition in vitro at a concentration that is relevant; no human studies have yet been conducted

Is a Form of


Caution Notice

May interact with enzymes of Drug Metabolism

Possible toxic effects (requires further study)

Examine.com Medical Disclaimer

Recommended doses of Hoodia Gorgonii tend to be around one gram of an extract of 70% steroidal glycosides or more, taken twice a day with each dose about an hour before a meal.

There is no evidence to suggest an optimal dose nor to support the above as being active, and the toxic dose in mice (as well as preliminary human evidence) is the exact same as the supplemental dose.


The Human Effect Matrix looks at human studies (excluding animal/petri-dish studies) to tell you what effect Hoodia gordonii has in your body, and how strong these effects are.
GradeLevel of Evidence
ARobust research conducted with repeated double blind clinical trials
BMultiple studies where at least two are double-blind and placebo controlled
CSingle double blind study or multiple cohort studies
DUncontrolled or observational studies only
Level of Evidence
EffectChange
Magnitude of Effect Size
Scientific ConsensusComments
CBlood Pressure

Notable

The increase in blood pressure noted with hoodia gordonii in otherwise healthy persons reached 5.9-15.9mmHg systolic and 4.6-11.5mmHg diastolic; a worrying increase

CHeart Rate

Minor

Both heart rate and pulse rate are increased with hoodia ingestion, which are thought to be related to toxic effects of the herb

CBilirubin

Minor

The increase in bilirubin seen with hoodia is thought to be a biomarker of possible hepatotoxicity, although it was not met with hemolysis (usually accompanies)

CLiver Enzymes

Minor

ALP was noted to be increased in otherwise healthy women given the standard dose of hoodia, although the other liver enzymes were not affected significantly

CLean Mass

No significant modifications in lean mass during weight loss with hoodia relative to placebo

CFat Mass

No significant reductions in fat mass are noted, secondary to a lack of influence on appetite

CWeight

No significant influence on overall body weight (due to no fluctuations in appetite and thus no significant fat loss)

CAppetite

No significant reduction in appetite was seen with hoodia relative to placebo


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Table of Contents:


Edit1. Sources and Composition

1.1. Sources

Hoodia gordonii (of the family Apocynaceae and formerly the Trichocaulon or Stapelia genera) is a small desert 'cactus' (actually part of the milkweed family[1]) that has traditional usage as a food product and thrist quencher in Africa[1][2] and has similar traditional usage and effects in the body as the related species hoodia pilifera[3] and similar bioactives to the forementioned and the officinale, currorii, and lugardii species.[4][5] The entire genera of Hoodia is sometimes known as veldkos (food from the veld) and due to its usage as a supplement hoodia gordonii may also be called Slimming Cactus.[6] When it blooms, the flowers give off the scent of raw meat which has led to the name of the flower sbeing carrion flowers.[1]

The hoodia plant is widely distributed in arid areas of South Africa and Namibia, and it is used as a food product due to its multi-stemmed succulent with thick, erect, cylindrical, fleshy and fairly hard, glabrous, grey-green to grey-brown stems; it is spiny, but not actually a cactus (cactuses are things in the Cactaceae family).[2] Hoodia gordonii appears to be a protected plant.[7]

The main bioactive appears to be able to be synthesized[8][7] although this may be subject to patent,[4] and industry specifications for hoodia gordonii growers suggest it should be at 0.3% of the plant's dry weight.[9]

Hoodia gordonii is a desert plant that resembles a cactus although it is not phylogenetically related to such. It is a vegetable more than anything, and appears to be traditionally used to suppress the desire to eat or drink water (similar to other famine foods such as Caralluma fimbriata)

1.2. Composition

Hoodia gordonii has some atypical methylated sugars in the glycosides including D-Thevetose (The), D-Cymarose (Cym), D-Oleandrose (Ole), D-digitoxose (Dig), and 3-O-methyl-6-deoxy-D-allose (MDA) as well as glucose;[2] these abbreviations are used below to illustrate the side chain, with the first one mentioned being the one connected to the basic steroid structure (either the molecule in the first bullet, or Calogenin).

The steroid glycosides contained in Hoodia include:

  • Hoodigogenin A and Gordonoside A, both are the same molecule (12β-tygloyl-14β-hydroxy-pregn-5-en-20-one) and form the base of all Gordonosides and most Hoodigosides (those not based on Calogenin)[10][11][12] and is sometimes also called Tigloyloxydigipurpurgenin II[3]
  • The glycoside based off of the aforementioned known as P57, P57A53, or Glycoside number 12 (Hg.12) with the glycoside chain of Cym-Cym-The;[3][2] known to have appetite suppressing properties, said to be at 0.3% (Industry Spec[9]) and measured from undetectable to 0.43% (4% of samples had over 0.3%[9] and elsewhere the dry weight of the plant itself was noted to be 0.24%[13])
  • Other Hoodigosides are based of the Hoodigogenin A structure and vary by their glycosides including Hoodigoside A (The-Cym), Hoodigoside B (The-The-Cym), Hoodigoside C (The-Cym-Cym-Cym), Hoodigoside D (The-The-Cym-Cym), Hoodigoside E (Glu-The-Cym-Cym), Hoodigoside F (Glu-Ole-The-Cym-Cym), Hoodigoside G (Glu-Cym-The-Cym-Cym), Hoodigoside H (Glu-Cym-Cym-Cym-Cym), Hoodigoside I (Glu-Ole-Cym-Cym-Cym), Hoodigoside J (Glu-Ole-Dig-Cym-Cym), Hoodigoside K (Glu-Glu-Cym)[11][2] Hoodigoside W (Ole-The-Cym-Cym), and Hoodigoside X (The-Cym-Cym)[14]
  • Gordonosides, which are also based off the Hoodigogenin A steroid. These include Gordonoside B (The-Ole-Cym-Cym), Gordonoside C (side chain unidentified), Gordonoside D (Dig-Ole-Cym-Cym), Gordonoside E (Ole-Ole-Cym-Cym), Gordonoside F (Ole-Cym-Cym-Cym), Gordonoside G (four Cyms), Gordonoside H (side chain unidentified), Gordonoside I (Dig-Ole-Ole-Cym-Cym), and Gordonoside L (Ole and four Cyms)[10][2]
  • Hoodigosides that are based off of Calogenin (pregn-5-ene-3β,14β,20β-triol) rather than Hoodigogenin A, but most have glucosides on the opposite side of the Calogenin chain. The most basic is Hoodigoside N (The-Ole; no secondary chain) and adding a diglucoside to the second site produces Hoodigoside M (The-Ole; Glu-Glu). All other structures have either an initial side chain of plus a tigloyl (Tig) group on the end and these include Hoodigoside V (The-Ole-Tig;Glu), Hoodigoside O (The-Ole-Tig;Glu-Glu), Hoodigoside L (The-Ole-Tig;Glu-Glu-Glu), Hoodigoside P (Ole-Cym-Tig;Glu-Glu-Glu), Hoodigoside R (Ole-Ole-Cym-Tig;Glu-Glu-Glu), Hoodigoside Q (Cym-Cym-The-Tig;Glu-Glu-Glu), Hoodignoside T (Cym-Cym-Cym-Ole-Tig;Glu-Glu), Hoodigoside S (Cym-Cym-Cym-Ole-Tig;Glu-Glu-Glu), Hoodigoside U (Cym-Cym-Cym-Cym-Tig;Glu-Glu-Glu)[15] Hoodigoside Y (The-Ole;Glu), and Hoodigoside Z (The-Cym-Cym;Glu-Tig)[14]
  • Unnamed Hoodigogenin A glycosides with the side chains Cym-The-Cym-Cym (18mg/kg),[3] Ole-Mda-Cym-Cym, Cym-Mda-Cym-Cym, Ole-Dig-Cym-Cym, and Ole-Cym-Cym-Cym[2]
  • Hoodistanalosides based on an Orostanol backbone (3,5,14,20-tetrahydroxy-5{6→7}abeo-pregnan-7-al[16]) of which the glycosides that exist are Hoodistanaloside A and Hoodistanaloside B, both with a similar glycoside chain (Tig-The-Ole;Glu) but differ by hydroxyls on the backbone[14]

Total steroids in the raw plant have been noted to reach 2.1% dry weight with P57 being about 11% of total steroids,[13] although supplements are usually standardized to much higher levels (33-80% steroidal glycosides).

Note: The above glycoside chains are named working outwards from the steroid, hence why P57 is listed as Cym-Cym-The while the picture below depicts The-Cym-Cym (as the chain extends out to the left)

The steroidal glycosides in Hoodia are either based off of Hoodigogenin A (synonymous with Gordonoside A) or they are based off of Calogenin. They only differ by what sugars (atypical methylated sugars) are included in their side chains and in what order they exist, having these sugars makes then 'glycosides' (without the sugars, they are 'aglycones' meaning 'without sugar')

Other constituents of Hoodia gordonii that do not fall in the steroidal glycoside category are:

  • Cholesterol and β-sitosterol (collectively 0.5% of an extract of 33% steroidal glycoside[17] or inclusive of stigmasterol they are at 0.39% of an 80% steroidal glycoside extract[18])
  • Fatty acids (collectively; palmitic, linolenic, oleic, stearic, arachidonic, behenic, henatriacontylic, lacceroic, psyllic, and geddic acids) at 20% of a 33% steroidal glycoside extract[17] or 3.12% of an 80% steroidal glycoside extract[18]
  • Alkanes (C31, C33) at 2.9% of a 33% steroidal glycoside extract[17]
  • Vitamin E (as alpha-tocopherol)[18]
The bioactives in Hoodia that do not belong to the steroidal glycosides are not well studied, and at this moment in time there does not appear to be anything remarkable about them; some of the saturated fatty acids get quite long though (34 carbons) which is mildly interesting

1.3. Physicochemical Properties

P57 is confirmed to activate the bitter receptor (TAS2R14).[19] Ligands of the bitter taste receptors tend to induce secretion of either GLP-1[20] or CCK,[21] and P57 has been noted to induce CCK as well.[19]

Hoodia is noted to activate the bitter taste receptors, which may have a gustatory influence on appetite regulation

Storage of hoodia gordonii extract at ambient temperature (21-24°C) less than 60% humidity for 19 months does not degrade the bioactive steroidal glycosides.[18]

Should be preserved at room temperature and normal humidity for little over a year and a half


Edit2. Pharmacology

2.1. Absorption

In vitro, intestinal absorption of P57 appears to be less than 2% when alongside Caco-2 cells at 100-200μM.[22] It appears to be taken up via P-glycoprotein and MRP transporters[23] and is subject to intestinal efflux;[24] the aglycone (Hoodigogenin A) is passively diffused.[25]

Bioavailability of steroidal glycosides (measured in P57 equivalents) in the pig intestine following ingestion of 7.9mg/kg of a hoodia gordonii extract (79.3% steroidal glycosides) appears to be in the range of 41.9-54.2% with a mean value of 46%.[26] Coingestion with a meal slowed the Tmax of the steroidal glycosides,[26] and a similar bioavailability has been noted in mice (47.5%).[27]

While the steroidal glycosides are not perfectly absorbed (and subject to intestinal efflux), there does appear to be absorption of the steroidal glycosides (as glycosides) which has reached 50% in pigs

Buccal absorption has been noted in vitro with P57, suggesting that oral absorption may be possible.[24]

A possible oral route of absorption appears to be possible with the main bioactive

2.2. Serum

In rats, 15mg/kg of isolated P57 has reached Cmax concentrations in the range of 0.1-3μM.[26]

In pigs, oral ingestion of 7.9mg/kg of steroidal glycosides (79.3% purity) has resulted in a Cmax of 73–115ng/mL P57 at a Tmax of 93-120 minutes.[26]

Oral ingestion of 1,110mg hoodia gordonii to females results noted a Cmax of steroidal glycosides of 92+/-47ng/mL after a Tmax of 45-50 minutes and a half-life of 50 minutes, conferring an AUC of 366-439ng/mL/h (with a trend for increased AUC after 15 days relative to a single dose).[28] The steroidal glycosides were measured in P57 equivalents.[28]

In humans, the standard recommended dose of hoodia appears to increase plamsa concentrations of steroidal glycosides to the low nanomolar range (although within the concentration range where it may act on the hypothalamus, assuming it reaches the brain in similar quantities)

2.3. Distribution

Oral ingestion of a hoodia gardonii extract (conferring 25mg/kg P57) to mice has been noted to increase tissue concentrations of P57 in the liver, intestines, and kidneys to a low level and there was no detectable increase in brain tissue.[27] The tissue:plasma ratios were calculated for the liver (0.02), intestines (0.11), and kidney (0.06) although none could be calculated for the brain.

P57 does not appear to be well distributed to tissues well following oral ingestion, and none has been detected in the brain (which is required for its supposed appetite suppressing effects, thought to be due to direct stimulation of the hypothalamus)

2.4. Metabolism

P57 appears to be metabolically stable in the presence of liver cells[23] but appears to be unstable in the stomach (45% degratation in 60 minutes) and moderately unstable in intestinal fluid (8% degradation in 120 minutes);[25] Hoodigogenin A tends to be formed when P57 is degraded, and it itself is stable under all conditions.[25]

P57 appears to be stable in liver cells but instable in the stomach, while the aglycone (Hoodigogenin A) appears to be stable in the stomach and intestines

2.5. Phase I Enzyme Interactions

P57 has been noted to inhibit CYP3A4 with an IC50 of 45μM while it has no inhibitory effect on CYP1A2, CYP2C9, and CYP2D6.[23] The aglycone, Hoodigogenin A, appears to be significantly more potent at inhibiting CYP3A4 with an IC50 of 3μM.[25]

Possible CYP3A4 inhibition may occur with Hoodigogenin A, and it is plausible that this may occur to a limited degree following oral ingestion of high doses of hoodia


Edit3. Cardiovascular Health

3.1. Cardiac Tissue

Supplementation of 1,110mg of hoodia gordonii (79.5% steroidal glycosides) was noted to increase pulse and heart rate relative to placebo when taken over 15 days alongside a controlled diet.[28]

An increase in pulse and heart rate has been noted with hoodia ingestion in otherwise healthy persons, which is thought to be associated with possible toxic effects (not clear at the moment)

3.2. Blood Pressure

Supplementation of 1,110mg of hoodia gordonii (79.5% steroidal glycosides) was noted to increase blood pressure relative to placebo when taken over 15 days alongside a controlled diet;[28] the magnitude of increase in these normotensive persons ranging from 5.9-15.9 (systolic) and 4.6-11.5mmHg (diastolic) on an individual basis.[28]

An increase in blood pressure has been noted with hoodia ingestion in otherwise healthy persons, but the magnitude of blood pressure increase is actually quite large and a concern


Edit4. Neurology

4.1. Appetite and Food Intake

Mechanistically, injections of isolated P57 into the rat hypothalamus have increased intracellular ATP concentrations which were associated with reductions in food intake (40-60%);[29] Hoodigogenin A appears to be inactive, and the increase in ATP is thought to underlie appetite reduction seen with P57.[29]

It is thought that P57 increases ATP concentration in the hypothalamus, which is a mechanism known to reduce appetite; this has been seen with intracerebral injections of P57 to rats

6.25–50mg/kg of P57e from hoodia gordonii over one week was able to reduce food intake with more potency on day one (49-55% reduction) than after seven days (12-45%) with irregular dose dependency;[3] 30mg/kg of this bioactive appeared to be more potent than 15mg/kg fenfluramine.[3]

One study mentions preclinical (unpublished) data from a trial where 1,800mg of a Hoodia gordonii extract (79.5% steroidal glycosides) taken twice daily for 15 days reduced appetite by 30% associated with a serum concentration of 100ng/mL total steroidal glycosides; when the authors themselves a trial in mildly overweight women given 1,110mg hoodia gordonii (79.3% steroidal glycosides, said to hit 100ng/mL) twice daily (hour before meals) in a clinical setting for 15 days failed to find significantly more appetite suppression with Hoodia (24%) than placebo (18%).[28]

Although one animal study (using oral supplementation rather than intracerebral injections) has noted positive effects, the human study has failed to outperform placebo


Edit5. Obesity and Fat Mass

5.1. Weight and Body Fat

In rats subject to 6.25-50mg/kg of the isolated pregnane triglycoside, body weight appears to be attenuated which is thought to be secondary to reduced food intake.[3]

In women given 1,110mg of the hoodia gordonii extract (79.5% steroidal glycosides) over 15 days, the lack of appetite suppression was met with a failure to decrease weight or body fat more than placebo.[28] There appear to be some small trials (not found online, but mentioned in this report[30]) which showed promise but were funded by PhytoPharm, a producer of Hoodia gordonii supplements.

Secondary to the influences on appetite (best evidence says that this does not occur to a large degree in humans) there are modifications in weight; no human evidence supports a weight loss effect of hoodia


Edit6. Interactions with Hormones

6.1. Corticosteroids

Pregnane glycosides from hoodia gordonii (25% purity) at 4-100µg/mL (IC50 in the range of 75-90µg/mL) is able to inhibit forskolin-induced secretion of corticosterone, with 100µg/mL needed to suppress secretion of cortisol or androstenedione.[31] It was noted to reduce HSD3B2 mRNA levels (no include on P450 enzymes nor StAR)

Inhibition of steroidogenesis from pregnane type steroids appears to be reduced 8-fold when the tigloyl group is added to C12, while glycosides on C3 (mostly D-cyamarose) seem to increase it.[31]

There may be an inhibitory effect on steroid synthesis in isolated adrenal cells with a high concentration of steroidal glycosides from Hoodia gordonii (may not be relevant following oral ingestion due to the high concentration)


Edit7. Safety and Toxicology

7.1. General

In mice, while 400mg/kg appears to be a well tolerated dose of hoodia gordonii (33% steroidal glycosides and 4.7% P57) it appears that 500-1,000mg/kg was associated with some mortality (none at the 750mg/kg dose oddly).[17]

There is apparent toxicity in mice at higher doses, which (if converted to human equivalents and standardized for the steroidal glycoside content) are within the ranges used for nutritional supplementation

Supplementation of 1,110mg of hoodia gordonii extract (79.5% steroidal glycosides) in women over 15 days has resulted in increased serum ALP (a liver enzyme) in the range of 4.7 to 8.8 U/L and was also able to increase total and indirect bilirubin by 0.20mg/dL to 0.58mg/dL and 0.18mg/dL to 0.49mg/dL (respectively).[28] The authors noted that they were unable to find a causative agent (either the steroidal glycosides of something in the unidentified 9.4% of the supplement), and due to no hemolysis nor inductions of other liver enzymes the clinical significance of these findings were uncertain.[28]

Limited human evidence has found changes in serum biomarkers that indicate toxicity, although at this moment the clinical relevance is unknown

7.2. Genotoxicity and Teratogenicity

Supplementation of 100-400mg/kg hoodia gordonii extract to mice (33% steroidal glycosides and 4.7% P57 overall) failed to exert genotoxic effects (higher doses not tested due to lethality with 1,000mg/kg).[17]

One mouse study (duplicated in Medline[32][33]) used 15-50mg/kg of hoodia gordonii extract (70% steroidal glycosides and 10% P57) during pregnancy noted reductions in maternal food intake associated with reductions in fetal size, with no noticeable effect from 5mg/kg. No dose of hoodia gordonii was associated with deformations to the fetus, nor was pregnancy state altered.

No apparent genotoxicity (damange to the DNA) nor teratogenicity (damage to the fetus), although this may be because higher doses were not tested due to killing mice

References

  1. Lee RA, Balick MJ. Indigenous use of Hoodia gordonii and appetite suppression. Explore (NY). (2007)
  2. van Heerden FR. Hoodia gordonii: a natural appetite suppressant. J Ethnopharmacol. (2008)
  3. van Heerden FR, et al. An appetite suppressant from Hoodia species. Phytochemistry. (2007)
  4. Pharmaceutical compositions having appetite suppressant activity
  5. Zhao J, et al. NMR fingerprinting for analysis of hoodia species and hoodia dietary products. Planta Med. (2011)
  6. Gathier G, et al. Forensic Identification of CITES Protected Slimming Cactus (Hoodia) Using DNA Barcoding. J Forensic Sci. (2013)
  7. Geoffroy P, et al. Synthesis of Hoodigogenin A, aglycone of natural appetite suppressant glycosteroids extracted from Hoodia gordonii. Steroids. (2011)
  8. Zhang J, et al. Expeditious synthesis of saponin P57, an appetite suppressant from Hoodia plants. Chem Commun (Camb). (2012)
  9. A rapid spectroscopic method for quantification of P57 in Hoodia gordonii raw material
  10. Dall'Acqua S, Innocenti G. Steroidal glycosides from Hoodia gordonii. Steroids. (2007)
  11. Pawar RS, et al. New oxypregnane glycosides from appetite suppressant herbal supplement Hoodia gordonii. Steroids. (2007)
  12. Shukla YJ, et al. Hoodigogenin A from Hoodia gordonii. Acta Crystallogr Sect E Struct Rep Online. (2008)
  13. Janssen HG, et al. Quantification of appetite suppressing steroid glycosides from Hoodia gordonii in dried plant material, purified extracts and food products using HPLC-UV and HPLC-MS methods. Anal Chim Acta. (2008)
  14. Shukla YJ, et al. Pregnane glycosides from Hoodia gordonii. Phytochemistry. (2009)
  15. Pawar RS, Shukla YJ, Khan IA. New calogenin glycosides from Hoodia gordonii. Steroids. (2007)
  16. Orostanal, a novel abeo-sterol inducing apoptosis in leukemia cell from a marine sponge, Stelletta hiwasaensis
  17. Scott AD, et al. Genotoxicity testing of a Hoodia gordonii extract. Food Chem Toxicol. (2012)
  18. Russell PJ, Swindells C. Chemical characterisation of Hoodia gordonii extract. Food Chem Toxicol. (2012)
  19. Le Nevé B, et al. The steroid glycoside H.g.-12 from Hoodia gordonii activates the human bitter receptor TAS2R14 and induces CCK release from HuTu-80 cells. Am J Physiol Gastrointest Liver Physiol. (2010)
  20. Dotson CD, et al. Bitter taste receptors influence glucose homeostasis. PLoS One. (2008)
  21. Chen MC, et al. Bitter stimuli induce Ca2+ signaling and CCK release in enteroendocrine STC-1 cells: role of L-type voltage-sensitive Ca2+ channels. Am J Physiol Cell Physiol. (2006)
  22. Madgula VL, et al. In vitro metabolic stability and intestinal transport of P57AS3 (P57) from Hoodia gordonii and its interaction with drug metabolizing enzymes. Planta Med. (2008)
  23. Greenfield SP, Fera M. The use of intravesical oxybutynin chloride in children with neurogenic bladder. J Urol. (1991)
  24. Vermaak I, et al. In vitro transport of the steroidal glycoside P57 from Hoodia gordonii across excised porcine intestinal and buccal tissue. Phytomedicine. (2011)
  25. Madgula VL, et al. Characterization of in vitro pharmacokinetic properties of hoodigogenin A from Hoodia gordonii. Planta Med. (2010)
  26. Absolute bioavailability of a Hoodia gordonii steroid glycoside from different physicochemical formats in the pig
  27. Madgula VL, et al. Bioavailability, pharmacokinetics, and tissue distribution of the oxypregnane steroidal glycoside P57AS3 (P57) from Hoodia gordonii in mouse model. Planta Med. (2010)
  28. Blom WA, et al. Effects of 15-d repeated consumption of Hoodia gordonii purified extract on safety, ad libitum energy intake, and body weight in healthy, overweight women: a randomized controlled trial. Am J Clin Nutr. (2011)
  29. MacLean DB, Luo LG. Increased ATP content/production in the hypothalamus may be a signal for energy-sensing of satiety: studies of the anorectic mechanism of a plant steroidal glycoside. Brain Res. (2004)
  30. Whelan AM, Jurgens TM, Szeto V. Case report. Efficacy of Hoodia for weight loss: is there evidence to support the efficacy claims. J Clin Pharm Ther. (2010)
  31. Komarnytsky S, et al. Pregnane glycosides interfere with steroidogenic enzymes to down-regulate corticosteroid production in human adrenocortical H295R cells. J Cell Physiol. (2013)
  32. Dent MP, et al. Safety profile of Hoodia gordonii extract: rabbit prenatal developmental toxicity study. Food Chem Toxicol. (2012)
  33. Dent MP, et al. Safety profile of Hoodia gordonii extract: mouse prenatal developmental toxicity study. Food Chem Toxicol. (2012)

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