virtualcyber
New Member
Did anyone try this product, LeptiGen from Avant Labs? Would love some feedback.
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LeptiGen
- Thread starter virtualcyber
- Start date
Blood&Iron
New Member
</span><table border="0" align="center" width="95%" cellpadding="3" cellspacing="1"><tr><td>Quote (virtualcyber @ June 24 2002,2:45)</td></tr><tr><td id="QUOTE">Did anyone try this product, LeptiGen from Avant Labs? Would love some feedback.[/QUOTE]<span id='postcolor'>
It ain't out yet.
It ain't out yet.
Blood&Iron
New Member
I preordered and received mine yesterday. I will not be using it for another 4 weeks or so, as I'm gonna bulk until the end of my current HST cycle. Par is only selling a prototype version at this point.
Par Deus listed the ingredients over on his board.
LeptiGen Ingredients: Vitamin E acetate powder, zinc gluconate, glucosamine
HCl, simmondsin, synephrine, calcium pyruvate, 5-HTP
The simmondsin sounds interesting. Pretty powerful appetite suppressor derived from jojoba plants. I'm not clear on the details of its action.
LeptiGen Ingredients: Vitamin E acetate powder, zinc gluconate, glucosamine
HCl, simmondsin, synephrine, calcium pyruvate, 5-HTP
The simmondsin sounds interesting. Pretty powerful appetite suppressor derived from jojoba plants. I'm not clear on the details of its action.
virtualcyber
New Member
Of all the stuff he has listed there, only one I don't know about is simmondsin and calcium pyruvate.
(1) vitamine E & zinc -- these are known to aid in raising leptin.
(2) glucosamine HCL -- See other glucosamine threads for info. Glucosamine sulfate, I believe, is the preferred form, not glucosamine HCL; these are not absorbed by body very well (only 10 - 20 %of powder).
(3) synephrine -- This has been known to speed leptin transport through blood-brain barrier.
==========================
Googling for simmondsin, it looks like an appetite and metabolism suppressant. I don't see why this would significantly contribute to leptin production.
calcium pyruvate allegedly aids in Kreb cycle ... I don't know about this one.
(1) vitamine E & zinc -- these are known to aid in raising leptin.
(2) glucosamine HCL -- See other glucosamine threads for info. Glucosamine sulfate, I believe, is the preferred form, not glucosamine HCL; these are not absorbed by body very well (only 10 - 20 %of powder).
(3) synephrine -- This has been known to speed leptin transport through blood-brain barrier.
==========================
Googling for simmondsin, it looks like an appetite and metabolism suppressant. I don't see why this would significantly contribute to leptin production.
calcium pyruvate allegedly aids in Kreb cycle ... I don't know about this one.
Blood&Iron
New Member
Info on simmondsin:
-----------------------------------------------------------------------------------
Unique Identifier
10744903
Medline Identifier
20211131
Authors
Flo G. Van Boven M. Vermaut S. Daenens P. Decuypere E. Cokelaere M.
Institution
Interdisciplinary Research Centre, Katholieke Universiteit Leuven, Belgium.
Title
The vagus nerve is involved in the anorexigenic effect of simmondsin in the rat.
Source
Appetite. 34(2):147-51, 2000 Apr.
Abstract
Simmondsin, 2-(cyanomethylene)-3 hydroxy 4,5 dimethoxy cyclohexyl beta-D-glucoside, from jojoba meal reduces food intake in rats. We investigated the mechanism of action simmondsin, by studying the effects of fasting or of vagotomy on the food intake reduction. The food intake reduction was significantly less in fasted rats than in non-fasted rats. The reduction of food intake was also significantly diminished after vagotomy. The results of the present experiments suggest that simmondsin reduces intake of food in rats through the augmentation of satiety, in part vagally mediated. Copyright 2000 Academic Press.
-------------------------------------------------------------------------------
Unique Identifier
10450335
Medline Identifier
99378829
Authors
Flo G. Vermaut S. Darras VM. Van Boven M. Decuypere E. Kuhn ER. Daenens P. Cokelaere M.
Institution
Interdisciplinary Research Center, Katholieke Universiteit Leuven, Afdeling Kortrijk, Belgium.
Title
Effects of simmondsin on food intake, growth, and metabolic variables in lean (+/?) and obese (fa/fa) Zucker rats.
Source
British Journal of Nutrition. 81(2):159-67, 1999 Feb.
Abstract
Incorporation of 2.5 g/kg of the anorexigen, simmondsin, in the diet resulted in food intake reduction in both lean and obese Zucker rats; however, the obese rats were much more sensitive to the food intake-reducing activity of simmondsin. In both obese and lean simmondsin-treated Zucker rats, growth was slower than in control rats, but was the same as that in pair-fed animals. The 24 h heat production pattern showed a smaller diurnal variation and a lower mean in obese rats than in lean rats. Food intake reduction, as a result of either simmondsin treatment or pair feeding, caused a decrease in mean heat production. Simmondsin treatment, but not pair feeding, caused a decrease in the diurnal variation of heat production. Plasma total cholesterol levels were increased in both simmondsin-treated and pair-fed obese and lean Zucker rats compared with control animals; this increase was mainly due to an increase in HDL-cholesterol levels. Blood leptin levels in both obese and lean rats decreased with decreased food intake and decreased fat deposition, but in obese rats, simmondsin treatment resulted in an additional decrease in leptin levels. It is concluded that the food intake-reducing effect of simmondsin is more pronounced in obese Zucker rats than in their lean littermates, and except for the simmondsin-specific effects on leptin and total cholesterol values in obese littermates, the effects of simmondsin are related to food intake restriction in obese and lean Zucker rats.
------------------------------------------------------------------------------------
The Journal of Nutrition Vol. 128 No. 12 December 1998, pp. 2669S-2670S
The Satiating Effect of a Diet Containing Jojoba Meal (Simmondsia chinensis) in Dogs1
Amanda J. Hawthorne2 and Richard F. Butterwick
Waltham Centre for Pet Nutrition, Waltham-on-the-Wolds, Melton Mowbray, Leicestershire, UK
INTRODUCTION
The seeds of jojoba (Simmondsia chinensis) are a source of stable long-chain wax-esters used primarily in cosmetics for their emollient properties, and sparingly as an industrial lubricant additive. The wax-esters constitute ~50% of the seed, whereas the remainder, defatted jojoba meal (JM),3 has only a few industrial applications. Defatted JM contains relatively large amounts of the unique cyanoglucosides, simmondsin, simmondsin ferrulate and other analogs. Several studies have attributed decreased food intake and weight loss to these compounds when ~10% defatted JM was included in the diet of rats (Cokelaere et al. 1992) and broiler hens (Arnouts et al. 1993). The aim of this study was to evaluate the effect of a diet containing 8% JM (equivalent to 0.5% simmondsin on a dry matter basis) on food intake and appetite suppression (satiety) in dogs.
Materials and methods. Twelve dogs of a variety of small and toy breeds and of various ages (6.6 ± 0.8 y) and weights (7.4 ± 1.3 kg) were divided into two groups that were balanced according to breed. All housing conditions and procedures fell within the U.K. Home Office regulations under conditions described in Loveridge (1994). The study was conducted over two 14-d test periods using a balanced cross-over design. The control diet © (Pedigree Chum original, Pedigree Petfoods, Melton Mowbray, Leicestershire, UK) was a manufactured, nutritionally complete canned diet for dogs. The test diet (CJ), consisted of the control diet plus 8% defatted JM on a dry matter basis (supplied by International Flora Technologies, Gilbert, AZ). Both were fed in amounts corresponding to calculated daily maintenance energy requirements (460 kJ/kg body weight0.75 on d 1), where diet C and defatted JM had energy contents of 0.40 and 1.36 MJ/100 g, respectively.
Because JM contained simmondsin and simmondsin-2-ferrulate at concentrations of 70.2 and 54.5 g/kg dry matter, respectively, addition of JM to diet C at 8% of dry matter achieved a final dietary concentration of 0.5% simmondsin on a dry matter basis.
Test periods were separated by a 14-d washout period during which dogs were fed an unlimited amount of a different variety of the same commercial canned dog food. During each 14-d period, food intake was recorded daily; body weight was recorded weekly.
On d 7 and 14 of each test period, appetite suppression (satiety) was assessed with the use of a challenge meal technique (Butterwick and Markwell 1997), in which a meal consisting of diet C was offered to the dogs exactly 3 h after the test diet was fed. Dogs were allowed unrestricted access to the challenge meal for 20 min after which food intake was recorded.
Repeated measures ANOVA was used to compare challenge meal intake, mean daily intake and body weight change of dogs fed diets C and CJ; significance was considered to be P < 0.05.
Results. Mean daily intake of diet CJ, on an absolute and an energy basis, was significantly (P < 0.001) lower than intake of diet C over the whole 14-d period (Table 1). The reduction in CJ intake was associated with a higher (P = 0.01) body weight loss for dogs consuming CJ (4.4 ± 0.9%) compared with C (1.5 ± 0.4%) over the 14-d period.
Mean challenge meal intake (d 7 and 14 combined) was significantly (P = 0.003) higher in dogs fed diet CJ compared with C (Table 2), largely due to the significantly higher intake ( P = 0.04) of the challenge meal after consumption of diet CJ compared with diet C on d 14. Challenge meal intakes were significantly (P = 0.03) lower in both groups on d 14 compared with d 7.
Because the challenge meal was offered exactly 3 h after the daily allowance had been consumed, and after at least 7 d of feeding the test diets, JM does not appear to increase satiety either immediately (3 h) or after long-term feeding (>24 h).
Discussion. In this study, a diet containing 8% defatted JM resulted in a reduction in food intake that was associated with a reduction, albeit small, in body weight. The association between body weight change and food intake suggests that lower energy intake is the principal driver of weight loss, although other mechanisms cannot be ruled out. However, the reduction in food and energy intake of diet CJ was relatively minor, representing a reduction of 8.5 and 5.7%, respectively, compared with diet C.
The absence of any satiating effect of JM and the presence of a significant increase in challenge meal intake may reflect energy compensation resulting from reduced energy intake of the test diet (CJ), or a sensory-taste response to a new food (diet C in the challenge meal). In this study, consumption of JM resulted in a reduction in mean food intake over the 14-d period with a gradual decrease beginning on d 3 of the study, indicating that there was no acute palatability response to JM. However, the complete absence of any reduction in challenge meal intake indicates that diet CJ has no profound effect on satiety. It is more likely that a gradual reduction in palatability or a learned aversion is the primary mechanism underlying reduced intake of JM.
Inclusion of JM in a standard commercial dog food did not appear to influence food intake through an effect on satiety because challenge meal intake did not decrease 3 h after consumption of the test diet. Results of this study suggest therefore that JM has limited application to diets designed for weight management.
FOOTNOTES
1 Presented as part of the Waltham International Symposium on Pet Nutrition and Health in the 21st Century, Orlando, FL, May 26-29, 1997. Guest editors for the symposium publication were Ivan Burger, Waltham Centre for Pet Nutrition, Leicestershire, UK and D'Ann Finley, University of California, Davis.
2 To whom correspondence should be addressed.
3 Abbreviations used:C, control diet: CJ, test diet; JM, jojoba meal.
LITERATURE CITED
Arnouts S., Buyse., Cokelaere M. M., Decuypere E. Jojoba meal (Simmondsia chinensis) in the diet of broiler breeder pullets: physiological and endocrinological effects. Poult. Sci. 1993; 72:1714-1721[Medline]
Butterwick R. F., Markwell P. J. Effect of amount and type of dietary fiber on food intake in energy-restricted dogs. Am. J. Vet. Res. 1997; 58:272-276[Medline]
Cokelaere M. M, Dangreau H. D., Arnouts S., Kuhn E. R., Decuypere E. M.-P. Influence of pure simmondsin on the food intake in rats. J. Agric. Food Chem. 1992; 40:1839-1842
Loveridge G. G. Provision of environmentally enriched housing for dogs. Anim. Technol. 1994; 45:1-19
-----------------------------------------------------------------------------
Unique Identifier
9761380
Medline Identifier
98432547
Authors
Flo G. Vermaut S. Van Boven M. Daenens P. Buyse J. Decuypere E. Kuhn E. Cokelaere M.
Institution
Interdisciplinary Research Centre, Katholieke Universiteit Leuven Campus Kortrijk, Belgium.
Title
Comparison of the effects of simmondsin and cholecystokinin on metabolism, brown adipose tissue and the pancreas in food-restricted rats.
Source
Hormone & Metabolic Research. 30(8):504-8, 1998 Aug.
Abstract
In this study, we investigated the analogies between the physiological effects of simmondsin, a satiety-inducing glycoside extracted from jojoba seeds, and the gastro-intestinal satiation peptide, cholecystokinin. The effects of intraperitoneal injection of the biological active CCK-octapeptide on the pancreas, interscapular brown adipose tissue, growth performance and energy metabolism in normal-fed, severely food intake-restricted (50 % of normal food intake) or moderately food intake-restricted (65 % of normal food intake) growing rats were compared to the effects of 0.25 % simmondsin mixed in the food, inducing moderate food intake reduction (65 % of normal) in rats. Cholecystokinin induced pancreatic hypertrophy. In normal fed rats, cholecystokinin had no effect on brown adipose tissue or growth, while, in severely food intake-restricted rats, it caused brown adipose tissue hypertrophy and reduced growth. In moderately food intake-restricted rats, both cholecystokinin and simmondsin induced pancreatic hypertrophy, increased brown adipose weight and metabolism and caused a slight decrease in growth. We conclude that cholecystokinin may decrease growth performance in fast growing severely food intake-restricted rats by stimulating brown adipose tissue metabolism, probably because of protein shortage induced by pancreatic hyperstimulation. Simmondsin has similar effects. These results support the hypothesis that endogenous cholecystokinin is involved in the effects of simmondsin in rats.
--------------------------------------------------------------------------------
Unique Identifier
8234131
Medline Identifier
94051954
Authors
Arnouts S. Buyse J. Cokelaere MM. Decuypere E.
Institution
Laboratory for Physiology and Immunology of Domestic Animals, Leuven, Belgium.
Title
Jojoba meal (Simmondsia chinensis) in the diet of broiler breeder pullets: physiological and endocrinological effects.
Source
Poultry Science. 72(9):1714-21, 1993 Sep.
Abstract
The present studies evaluated the ability of jojoba meal (JO) to inhibit feed intake of broiler breeder pullets to limit body weight gain as recommended by the breeder company. A first experiment, using graded levels of JO supplementation (0 to 12%), was conducted to establish appropriate JO supplementation. Adequate reduction of growth rate was obtained with 4% JO supplementation. However, notwithstanding their similar growth rate, 4% JO chickens consumed considerably more feed compared with feed-restricted chickens. The dose-dependent impairment of feed intake with increasing levels of JO supplementation was also associated with increased plasma growth hormone and thyroxine and with decreased plasma insulin-like growth factor-I and triiodothyronine concentrations compared with 0% JO chickens. A second experiment included a pair-fed group. Notwithstanding their similar feed intake, 4% JO chickens gained significantly less body weight compared with their pair-fed counterparts. The 4% JO chickens also had a longer feed transit time per kilogram body weight. Again, circulating levels of the somatotrophic and thyrotrophic hormones were altered according to the dietary treatment. From all these observations, it was concluded that the growth retardation caused by JO supplementation was provoked by an inhibition of appetite linked with the simmondsin content of JO as well as by other antinutritional compounds affecting digestibility.
-----------------------------------------------------------------------------------
Unique Identifier
10744903
Medline Identifier
20211131
Authors
Flo G. Van Boven M. Vermaut S. Daenens P. Decuypere E. Cokelaere M.
Institution
Interdisciplinary Research Centre, Katholieke Universiteit Leuven, Belgium.
Title
The vagus nerve is involved in the anorexigenic effect of simmondsin in the rat.
Source
Appetite. 34(2):147-51, 2000 Apr.
Abstract
Simmondsin, 2-(cyanomethylene)-3 hydroxy 4,5 dimethoxy cyclohexyl beta-D-glucoside, from jojoba meal reduces food intake in rats. We investigated the mechanism of action simmondsin, by studying the effects of fasting or of vagotomy on the food intake reduction. The food intake reduction was significantly less in fasted rats than in non-fasted rats. The reduction of food intake was also significantly diminished after vagotomy. The results of the present experiments suggest that simmondsin reduces intake of food in rats through the augmentation of satiety, in part vagally mediated. Copyright 2000 Academic Press.
-------------------------------------------------------------------------------
Unique Identifier
10450335
Medline Identifier
99378829
Authors
Flo G. Vermaut S. Darras VM. Van Boven M. Decuypere E. Kuhn ER. Daenens P. Cokelaere M.
Institution
Interdisciplinary Research Center, Katholieke Universiteit Leuven, Afdeling Kortrijk, Belgium.
Title
Effects of simmondsin on food intake, growth, and metabolic variables in lean (+/?) and obese (fa/fa) Zucker rats.
Source
British Journal of Nutrition. 81(2):159-67, 1999 Feb.
Abstract
Incorporation of 2.5 g/kg of the anorexigen, simmondsin, in the diet resulted in food intake reduction in both lean and obese Zucker rats; however, the obese rats were much more sensitive to the food intake-reducing activity of simmondsin. In both obese and lean simmondsin-treated Zucker rats, growth was slower than in control rats, but was the same as that in pair-fed animals. The 24 h heat production pattern showed a smaller diurnal variation and a lower mean in obese rats than in lean rats. Food intake reduction, as a result of either simmondsin treatment or pair feeding, caused a decrease in mean heat production. Simmondsin treatment, but not pair feeding, caused a decrease in the diurnal variation of heat production. Plasma total cholesterol levels were increased in both simmondsin-treated and pair-fed obese and lean Zucker rats compared with control animals; this increase was mainly due to an increase in HDL-cholesterol levels. Blood leptin levels in both obese and lean rats decreased with decreased food intake and decreased fat deposition, but in obese rats, simmondsin treatment resulted in an additional decrease in leptin levels. It is concluded that the food intake-reducing effect of simmondsin is more pronounced in obese Zucker rats than in their lean littermates, and except for the simmondsin-specific effects on leptin and total cholesterol values in obese littermates, the effects of simmondsin are related to food intake restriction in obese and lean Zucker rats.
------------------------------------------------------------------------------------
The Journal of Nutrition Vol. 128 No. 12 December 1998, pp. 2669S-2670S
The Satiating Effect of a Diet Containing Jojoba Meal (Simmondsia chinensis) in Dogs1
Amanda J. Hawthorne2 and Richard F. Butterwick
Waltham Centre for Pet Nutrition, Waltham-on-the-Wolds, Melton Mowbray, Leicestershire, UK
INTRODUCTION
The seeds of jojoba (Simmondsia chinensis) are a source of stable long-chain wax-esters used primarily in cosmetics for their emollient properties, and sparingly as an industrial lubricant additive. The wax-esters constitute ~50% of the seed, whereas the remainder, defatted jojoba meal (JM),3 has only a few industrial applications. Defatted JM contains relatively large amounts of the unique cyanoglucosides, simmondsin, simmondsin ferrulate and other analogs. Several studies have attributed decreased food intake and weight loss to these compounds when ~10% defatted JM was included in the diet of rats (Cokelaere et al. 1992) and broiler hens (Arnouts et al. 1993). The aim of this study was to evaluate the effect of a diet containing 8% JM (equivalent to 0.5% simmondsin on a dry matter basis) on food intake and appetite suppression (satiety) in dogs.
Materials and methods. Twelve dogs of a variety of small and toy breeds and of various ages (6.6 ± 0.8 y) and weights (7.4 ± 1.3 kg) were divided into two groups that were balanced according to breed. All housing conditions and procedures fell within the U.K. Home Office regulations under conditions described in Loveridge (1994). The study was conducted over two 14-d test periods using a balanced cross-over design. The control diet © (Pedigree Chum original, Pedigree Petfoods, Melton Mowbray, Leicestershire, UK) was a manufactured, nutritionally complete canned diet for dogs. The test diet (CJ), consisted of the control diet plus 8% defatted JM on a dry matter basis (supplied by International Flora Technologies, Gilbert, AZ). Both were fed in amounts corresponding to calculated daily maintenance energy requirements (460 kJ/kg body weight0.75 on d 1), where diet C and defatted JM had energy contents of 0.40 and 1.36 MJ/100 g, respectively.
Because JM contained simmondsin and simmondsin-2-ferrulate at concentrations of 70.2 and 54.5 g/kg dry matter, respectively, addition of JM to diet C at 8% of dry matter achieved a final dietary concentration of 0.5% simmondsin on a dry matter basis.
Test periods were separated by a 14-d washout period during which dogs were fed an unlimited amount of a different variety of the same commercial canned dog food. During each 14-d period, food intake was recorded daily; body weight was recorded weekly.
On d 7 and 14 of each test period, appetite suppression (satiety) was assessed with the use of a challenge meal technique (Butterwick and Markwell 1997), in which a meal consisting of diet C was offered to the dogs exactly 3 h after the test diet was fed. Dogs were allowed unrestricted access to the challenge meal for 20 min after which food intake was recorded.
Repeated measures ANOVA was used to compare challenge meal intake, mean daily intake and body weight change of dogs fed diets C and CJ; significance was considered to be P < 0.05.
Results. Mean daily intake of diet CJ, on an absolute and an energy basis, was significantly (P < 0.001) lower than intake of diet C over the whole 14-d period (Table 1). The reduction in CJ intake was associated with a higher (P = 0.01) body weight loss for dogs consuming CJ (4.4 ± 0.9%) compared with C (1.5 ± 0.4%) over the 14-d period.
Mean challenge meal intake (d 7 and 14 combined) was significantly (P = 0.003) higher in dogs fed diet CJ compared with C (Table 2), largely due to the significantly higher intake ( P = 0.04) of the challenge meal after consumption of diet CJ compared with diet C on d 14. Challenge meal intakes were significantly (P = 0.03) lower in both groups on d 14 compared with d 7.
Because the challenge meal was offered exactly 3 h after the daily allowance had been consumed, and after at least 7 d of feeding the test diets, JM does not appear to increase satiety either immediately (3 h) or after long-term feeding (>24 h).
Discussion. In this study, a diet containing 8% defatted JM resulted in a reduction in food intake that was associated with a reduction, albeit small, in body weight. The association between body weight change and food intake suggests that lower energy intake is the principal driver of weight loss, although other mechanisms cannot be ruled out. However, the reduction in food and energy intake of diet CJ was relatively minor, representing a reduction of 8.5 and 5.7%, respectively, compared with diet C.
The absence of any satiating effect of JM and the presence of a significant increase in challenge meal intake may reflect energy compensation resulting from reduced energy intake of the test diet (CJ), or a sensory-taste response to a new food (diet C in the challenge meal). In this study, consumption of JM resulted in a reduction in mean food intake over the 14-d period with a gradual decrease beginning on d 3 of the study, indicating that there was no acute palatability response to JM. However, the complete absence of any reduction in challenge meal intake indicates that diet CJ has no profound effect on satiety. It is more likely that a gradual reduction in palatability or a learned aversion is the primary mechanism underlying reduced intake of JM.
Inclusion of JM in a standard commercial dog food did not appear to influence food intake through an effect on satiety because challenge meal intake did not decrease 3 h after consumption of the test diet. Results of this study suggest therefore that JM has limited application to diets designed for weight management.
FOOTNOTES
1 Presented as part of the Waltham International Symposium on Pet Nutrition and Health in the 21st Century, Orlando, FL, May 26-29, 1997. Guest editors for the symposium publication were Ivan Burger, Waltham Centre for Pet Nutrition, Leicestershire, UK and D'Ann Finley, University of California, Davis.
2 To whom correspondence should be addressed.
3 Abbreviations used:C, control diet: CJ, test diet; JM, jojoba meal.
LITERATURE CITED
Arnouts S., Buyse., Cokelaere M. M., Decuypere E. Jojoba meal (Simmondsia chinensis) in the diet of broiler breeder pullets: physiological and endocrinological effects. Poult. Sci. 1993; 72:1714-1721[Medline]
Butterwick R. F., Markwell P. J. Effect of amount and type of dietary fiber on food intake in energy-restricted dogs. Am. J. Vet. Res. 1997; 58:272-276[Medline]
Cokelaere M. M, Dangreau H. D., Arnouts S., Kuhn E. R., Decuypere E. M.-P. Influence of pure simmondsin on the food intake in rats. J. Agric. Food Chem. 1992; 40:1839-1842
Loveridge G. G. Provision of environmentally enriched housing for dogs. Anim. Technol. 1994; 45:1-19
-----------------------------------------------------------------------------
Unique Identifier
9761380
Medline Identifier
98432547
Authors
Flo G. Vermaut S. Van Boven M. Daenens P. Buyse J. Decuypere E. Kuhn E. Cokelaere M.
Institution
Interdisciplinary Research Centre, Katholieke Universiteit Leuven Campus Kortrijk, Belgium.
Title
Comparison of the effects of simmondsin and cholecystokinin on metabolism, brown adipose tissue and the pancreas in food-restricted rats.
Source
Hormone & Metabolic Research. 30(8):504-8, 1998 Aug.
Abstract
In this study, we investigated the analogies between the physiological effects of simmondsin, a satiety-inducing glycoside extracted from jojoba seeds, and the gastro-intestinal satiation peptide, cholecystokinin. The effects of intraperitoneal injection of the biological active CCK-octapeptide on the pancreas, interscapular brown adipose tissue, growth performance and energy metabolism in normal-fed, severely food intake-restricted (50 % of normal food intake) or moderately food intake-restricted (65 % of normal food intake) growing rats were compared to the effects of 0.25 % simmondsin mixed in the food, inducing moderate food intake reduction (65 % of normal) in rats. Cholecystokinin induced pancreatic hypertrophy. In normal fed rats, cholecystokinin had no effect on brown adipose tissue or growth, while, in severely food intake-restricted rats, it caused brown adipose tissue hypertrophy and reduced growth. In moderately food intake-restricted rats, both cholecystokinin and simmondsin induced pancreatic hypertrophy, increased brown adipose weight and metabolism and caused a slight decrease in growth. We conclude that cholecystokinin may decrease growth performance in fast growing severely food intake-restricted rats by stimulating brown adipose tissue metabolism, probably because of protein shortage induced by pancreatic hyperstimulation. Simmondsin has similar effects. These results support the hypothesis that endogenous cholecystokinin is involved in the effects of simmondsin in rats.
--------------------------------------------------------------------------------
Unique Identifier
8234131
Medline Identifier
94051954
Authors
Arnouts S. Buyse J. Cokelaere MM. Decuypere E.
Institution
Laboratory for Physiology and Immunology of Domestic Animals, Leuven, Belgium.
Title
Jojoba meal (Simmondsia chinensis) in the diet of broiler breeder pullets: physiological and endocrinological effects.
Source
Poultry Science. 72(9):1714-21, 1993 Sep.
Abstract
The present studies evaluated the ability of jojoba meal (JO) to inhibit feed intake of broiler breeder pullets to limit body weight gain as recommended by the breeder company. A first experiment, using graded levels of JO supplementation (0 to 12%), was conducted to establish appropriate JO supplementation. Adequate reduction of growth rate was obtained with 4% JO supplementation. However, notwithstanding their similar growth rate, 4% JO chickens consumed considerably more feed compared with feed-restricted chickens. The dose-dependent impairment of feed intake with increasing levels of JO supplementation was also associated with increased plasma growth hormone and thyroxine and with decreased plasma insulin-like growth factor-I and triiodothyronine concentrations compared with 0% JO chickens. A second experiment included a pair-fed group. Notwithstanding their similar feed intake, 4% JO chickens gained significantly less body weight compared with their pair-fed counterparts. The 4% JO chickens also had a longer feed transit time per kilogram body weight. Again, circulating levels of the somatotrophic and thyrotrophic hormones were altered according to the dietary treatment. From all these observations, it was concluded that the growth retardation caused by JO supplementation was provoked by an inhibition of appetite linked with the simmondsin content of JO as well as by other antinutritional compounds affecting digestibility.
virtualcyber
New Member
Just in case someone is interested ... let me summarize what has been posted about LeptiGen and its probably most active ingredient, glucosamine.
For those interested in experimenting a bit with glucosamine, here is the relevant information:
==========================================
(1) Dosing
A simple calculation shows that 185 lb person needs to ingest approximately 2.25 grams of glucosamine HCL to raise leptin level by about 20% in lean folks and by about 75% in obese people (assuming that _in vitro_ and _in vivo_ experiments would result in the same "environment" for glucosamine to affect leptin level, provided the same level of glucosamine concentration exists in both experiments -- which is a big assumption).
The calculation is based on (a) bioavailability (44%) of orally ingested glucosamine, (b) average blood volume in 185 lb human and © the concentration of glucosamine used in the experiment described in the following reference:
"Hexosamines regulate leptin production in human subcutaneous adipocytes"
by Considine RV, Cooksey RC, Williams LB, Fawcett RL, Zhang P, Ambrosius WT, Whitfield RM, Jones R, Inman M, Huse J, McClain DA. Related Articles
========================================
(2) Glucosamine HCL and pharmacokinetics
Half life ~ 58 h
Bioavailability ~44% (liver burns 45%, 11% eliminated via
faecal waste material)
The above information and more can be found in
"Absorption, distribution, metabolism and excretion of glucosamine sulfate. A review."
by Setnikar I, Rovati LC.
For those interested in experimenting a bit with glucosamine, here is the relevant information:
==========================================
(1) Dosing
A simple calculation shows that 185 lb person needs to ingest approximately 2.25 grams of glucosamine HCL to raise leptin level by about 20% in lean folks and by about 75% in obese people (assuming that _in vitro_ and _in vivo_ experiments would result in the same "environment" for glucosamine to affect leptin level, provided the same level of glucosamine concentration exists in both experiments -- which is a big assumption).
The calculation is based on (a) bioavailability (44%) of orally ingested glucosamine, (b) average blood volume in 185 lb human and © the concentration of glucosamine used in the experiment described in the following reference:
"Hexosamines regulate leptin production in human subcutaneous adipocytes"
by Considine RV, Cooksey RC, Williams LB, Fawcett RL, Zhang P, Ambrosius WT, Whitfield RM, Jones R, Inman M, Huse J, McClain DA. Related Articles
========================================
(2) Glucosamine HCL and pharmacokinetics
Half life ~ 58 h
Bioavailability ~44% (liver burns 45%, 11% eliminated via
faecal waste material)
The above information and more can be found in
"Absorption, distribution, metabolism and excretion of glucosamine sulfate. A review."
by Setnikar I, Rovati LC.