Please Scroll Down to See Forums Below macrophage69alpha
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yes. its called hyperplasia and it does occur in adults
green tea extract
- Thread starter dzuljas
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I know what hyperplasia is and it does nothing to add to your argument.macrophage69alpha said:
Do you have a reference to support your claim that adults can grow new fat cells?
I'm not saying that they can't, but if they can, it's a new addition to my knowledge. I'm sure a LOT has changed since I went through medical school.
macrophage69alpha
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merely posted a study....was not making an argument.. you were, when you said that humans dont form new adipocytes (hyperplasia) and that fat gain is on through fat cell size increases (hypertrophy).
and to answer again, yes either you were given incorrect information or that information has changed/been corrected (however fat cell hyperplasia was established in animal models in the 60's)
1: Zhonghua Zheng Xing Shao Shang Wai Ke Za Zhi. 1999 May;15(3):199-201. Links
[Human preadipocyte culture and the establishment of hyperplasia and hypertrophy model][Article in Chinese]
Zhu X, He Q, Lin Z.
Department of Plastic and Reconstructive Surgery, Second Military Medical University, Shanghai 200003.
OBJECTIVE: To better understand hyperplasia and hypertrophy properties of human adipose tissue. METHODS: Using an "adhesion-ceiling" culture strategy, fibroblast-like cells from adult pure adipose granules were successfully cultured. RESULTS: The cells were highly homogeneous, highly proliferative and with a high differentiation rate. Their dynamic morphological changes, growth curve, glycerophosphate dehydrogenase pattern, oil red O staining, and reaction to insulin and dexamethasone all verified their preadipocyte identity. Under controlled conditions, the preadipocytes replayed their in vivo hyperplasia and hypertrophy process. CONCLUSION: In mature human adipose tissue there exist functionally active fractions that can be modified. This study laid the basis for further probing into obesity and fat autotransplantation.
1: J Clin Endocrinol Metab. 2005 Nov;90(11):6207-13. Epub 2005 Aug 30. Links
Long-term prospective and controlled studies demonstrate adipose tissue hypercellularity and relative leptin deficiency in the postobese state.Lofgren P, Andersson I, Adolfsson B, Leijonhufvud BM, Hertel K, Hoffstedt J, Arner P.
Department of Medicine, Karolinska University Hospital Huddinge, SE-141 86 Huddinge, Stockholm, Sweden.
CONTEXT: Enlarged fat cells and leptin hypersecretion are hallmarks of common obesity. OBJECTIVE: The objective of this study was to investigate fat cell size and leptin production in the basal state after long-term steady-state weight reduction to the nonobese state. DESIGN: This prospective case-control study had a duration of 3 +/- 1 (mean +/- sd) yr. PATIENTS: Twenty-five obese women (cases) were studied. Each case was compared with a control subject matched for age, sex, and body mass index (BMI) at nadir of weight for the cases. SETTING: This study was conducted at Karolinska University Hospital (Stockholm, Sweden). INTERVENTION: The subjects were followed until they reached a steady-state weight reduction after lifestyle modification or bariatric surgery (cases). Treatment target was the nonobese state (BMI < 30 kg/m2). Subcutaneous adipose tissue secretion of leptin, serum leptin levels, and fat cell volume were determined after an overnight fast. RESULTS: Ten obese women (40%) reached the nonobese state. This was accompanied by marked decreases in fat cell volume, leptin secretion, and serum leptin concentrations (P < 0.0001). The postobese cases had 43% smaller fat cell volume (P = 0.0008), 68% lower adipocyte leptin production (P = 0.001), and 54% lower serum leptin levels (P = 0.0007) than control subjects, despite almost identical percent body fat in the two groups. Fat cell volume, but not percent body fat or BMI, was directly proportional to leptin secretion and serum leptin concentrations. CONCLUSION: Adipose tissue hyperplasia (too many small fat cells) and low leptin production resulting in relative hypoleptinemia in the fasting (basal) state are common features of the postobese state in women.
1: FASEB J. 2004 Dec;18(15):1925-7. Epub 2004 Oct 6. Links
Loss of cyclin-dependent kinase inhibitors produces adipocyte hyperplasia and obesity.Naaz A, Holsberger DR, Iwamoto GA, Nelson A, Kiyokawa H, Cooke PS.
Department of Veterinary Biosciences, University of Illinois-Urbana, Urbana, Illinois 61802, USA.
Adipocyte hyperplasia is characteristic of some forms of human obesity, but the role of adipocyte number in obesity and how normal adipocyte number is established are unclear. Preadipocytes proliferate and then differentiate to become mitotically quiescent adipocytes. This involves exit from the cell cycle, a process regulated by cell cycle inhibitors such as the cyclin-dependent kinase inhibitors (CDKIs) p27 and p21. 3T3-L1 preadipocytes show marked changes in p27 and p21 during differentiation, suggesting CDKIs may regulate establishment of adipocyte number in vivo. To study the role of these CDKIs in adipogenesis, we analyzed adult p27 knockout (p27KO), p21 knockout (p21KO), p27/p21 double knockout (DBKO), and wild-type (WT) mice. Adult DBKO mice weighed 100% more and had fourfold increases in body fat percentage compared with WT. Fat pad weights were increased 80, 90, and 500% in p27KO, p21KO, and DBKO mice, respectively, compared with WT. Adipocyte numbers of p27KO, p21KO, and DBKO mice were 1.9-, 1.7-, and 6.1-fold, respectively, that of WT; adipocyte size was not increased. DBKO mice showed glucose intolerance, insulin insensitivity, hepatic steatosis and dyslipidemia; gradations of these effects occurred in p27KO and p21KO mice. In conclusion, p27KO and p21KO mice are obese because of adipocyte hyperplasia, and DBKO mice have further increases in obesity and adipocyte hyperplasia, indicating that their functions in establishing adipocyte number are not redundant. p27 and p21 are major regulators of adipocyte number in vivo, and knockouts lacking one or both of these proteins provide models for producing adipocyte hyperplasia and understanding its metabolic consequences.
1: J Clin Invest. 1987 Feb;79(2):632-6. Links
Release of mitogenic factors by cultured preadipocytes from massively obese human subjects.Lau DC, Roncari DA, Hollenberg CH.
In this study, possible paracrine factors in adipose tissue from lean and obese subjects were sought. Conditioned media were prepared by incubation in alpha minimum essential medium of adipocyte precursors derived from lean and massively obese subjects. Adipocyte-precursor-derived conditioned media from the obese stimulated replication of cultured rat perirenal adipocyte precursors by about fourfold over control. The effect of media conditioned by precursors derived from lean subjects was much less evident. The mitogenicity of conditioned media was abolished by trypsin, indicating the protein nature of the mitogenic factor(s). Sephacryl S-200 chromatography of adipocyte-precursor-derived conditioned media from obese subjects revealed one major active fraction with molecular masses in the range of 25,000-40,000. Our results demonstrate that adipocyte precursors derived from massively obese subjects release factors mitogenic on cultured rat adipocyte precursors. These principles may act as paracrine factors contributing to the development of the adipocyte hyperplasia characteristic of massive obesity.
and to answer again, yes either you were given incorrect information or that information has changed/been corrected (however fat cell hyperplasia was established in animal models in the 60's)
1: Zhonghua Zheng Xing Shao Shang Wai Ke Za Zhi. 1999 May;15(3):199-201. Links
[Human preadipocyte culture and the establishment of hyperplasia and hypertrophy model][Article in Chinese]
Zhu X, He Q, Lin Z.
Department of Plastic and Reconstructive Surgery, Second Military Medical University, Shanghai 200003.
OBJECTIVE: To better understand hyperplasia and hypertrophy properties of human adipose tissue. METHODS: Using an "adhesion-ceiling" culture strategy, fibroblast-like cells from adult pure adipose granules were successfully cultured. RESULTS: The cells were highly homogeneous, highly proliferative and with a high differentiation rate. Their dynamic morphological changes, growth curve, glycerophosphate dehydrogenase pattern, oil red O staining, and reaction to insulin and dexamethasone all verified their preadipocyte identity. Under controlled conditions, the preadipocytes replayed their in vivo hyperplasia and hypertrophy process. CONCLUSION: In mature human adipose tissue there exist functionally active fractions that can be modified. This study laid the basis for further probing into obesity and fat autotransplantation.
1: J Clin Endocrinol Metab. 2005 Nov;90(11):6207-13. Epub 2005 Aug 30. Links
Long-term prospective and controlled studies demonstrate adipose tissue hypercellularity and relative leptin deficiency in the postobese state.Lofgren P, Andersson I, Adolfsson B, Leijonhufvud BM, Hertel K, Hoffstedt J, Arner P.
Department of Medicine, Karolinska University Hospital Huddinge, SE-141 86 Huddinge, Stockholm, Sweden.
CONTEXT: Enlarged fat cells and leptin hypersecretion are hallmarks of common obesity. OBJECTIVE: The objective of this study was to investigate fat cell size and leptin production in the basal state after long-term steady-state weight reduction to the nonobese state. DESIGN: This prospective case-control study had a duration of 3 +/- 1 (mean +/- sd) yr. PATIENTS: Twenty-five obese women (cases) were studied. Each case was compared with a control subject matched for age, sex, and body mass index (BMI) at nadir of weight for the cases. SETTING: This study was conducted at Karolinska University Hospital (Stockholm, Sweden). INTERVENTION: The subjects were followed until they reached a steady-state weight reduction after lifestyle modification or bariatric surgery (cases). Treatment target was the nonobese state (BMI < 30 kg/m2). Subcutaneous adipose tissue secretion of leptin, serum leptin levels, and fat cell volume were determined after an overnight fast. RESULTS: Ten obese women (40%) reached the nonobese state. This was accompanied by marked decreases in fat cell volume, leptin secretion, and serum leptin concentrations (P < 0.0001). The postobese cases had 43% smaller fat cell volume (P = 0.0008), 68% lower adipocyte leptin production (P = 0.001), and 54% lower serum leptin levels (P = 0.0007) than control subjects, despite almost identical percent body fat in the two groups. Fat cell volume, but not percent body fat or BMI, was directly proportional to leptin secretion and serum leptin concentrations. CONCLUSION: Adipose tissue hyperplasia (too many small fat cells) and low leptin production resulting in relative hypoleptinemia in the fasting (basal) state are common features of the postobese state in women.
1: FASEB J. 2004 Dec;18(15):1925-7. Epub 2004 Oct 6. Links
Loss of cyclin-dependent kinase inhibitors produces adipocyte hyperplasia and obesity.Naaz A, Holsberger DR, Iwamoto GA, Nelson A, Kiyokawa H, Cooke PS.
Department of Veterinary Biosciences, University of Illinois-Urbana, Urbana, Illinois 61802, USA.
Adipocyte hyperplasia is characteristic of some forms of human obesity, but the role of adipocyte number in obesity and how normal adipocyte number is established are unclear. Preadipocytes proliferate and then differentiate to become mitotically quiescent adipocytes. This involves exit from the cell cycle, a process regulated by cell cycle inhibitors such as the cyclin-dependent kinase inhibitors (CDKIs) p27 and p21. 3T3-L1 preadipocytes show marked changes in p27 and p21 during differentiation, suggesting CDKIs may regulate establishment of adipocyte number in vivo. To study the role of these CDKIs in adipogenesis, we analyzed adult p27 knockout (p27KO), p21 knockout (p21KO), p27/p21 double knockout (DBKO), and wild-type (WT) mice. Adult DBKO mice weighed 100% more and had fourfold increases in body fat percentage compared with WT. Fat pad weights were increased 80, 90, and 500% in p27KO, p21KO, and DBKO mice, respectively, compared with WT. Adipocyte numbers of p27KO, p21KO, and DBKO mice were 1.9-, 1.7-, and 6.1-fold, respectively, that of WT; adipocyte size was not increased. DBKO mice showed glucose intolerance, insulin insensitivity, hepatic steatosis and dyslipidemia; gradations of these effects occurred in p27KO and p21KO mice. In conclusion, p27KO and p21KO mice are obese because of adipocyte hyperplasia, and DBKO mice have further increases in obesity and adipocyte hyperplasia, indicating that their functions in establishing adipocyte number are not redundant. p27 and p21 are major regulators of adipocyte number in vivo, and knockouts lacking one or both of these proteins provide models for producing adipocyte hyperplasia and understanding its metabolic consequences.
1: J Clin Invest. 1987 Feb;79(2):632-6. Links
Release of mitogenic factors by cultured preadipocytes from massively obese human subjects.Lau DC, Roncari DA, Hollenberg CH.
In this study, possible paracrine factors in adipose tissue from lean and obese subjects were sought. Conditioned media were prepared by incubation in alpha minimum essential medium of adipocyte precursors derived from lean and massively obese subjects. Adipocyte-precursor-derived conditioned media from the obese stimulated replication of cultured rat perirenal adipocyte precursors by about fourfold over control. The effect of media conditioned by precursors derived from lean subjects was much less evident. The mitogenicity of conditioned media was abolished by trypsin, indicating the protein nature of the mitogenic factor(s). Sephacryl S-200 chromatography of adipocyte-precursor-derived conditioned media from obese subjects revealed one major active fraction with molecular masses in the range of 25,000-40,000. Our results demonstrate that adipocyte precursors derived from massively obese subjects release factors mitogenic on cultured rat adipocyte precursors. These principles may act as paracrine factors contributing to the development of the adipocyte hyperplasia characteristic of massive obesity.
macrophage69alpha
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Dance Princess
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Does Anyone Find That Green Tea Lowers Their Electrolytes If It Is Taken During Or Before Cardio? I Got A Very Weak Feeling-nearly Passing Out-so I Started Either Breaking A Egg In It Or Putting Protein Powder In It-and It Is Fine. I Am Just Guessing That My Electolytes Were Low.
macrophage69alpha
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can affect your blood sugar, it is has been shown to increase glucose uptake. but as far as affecting your electroytes, there is no clinical evidence of that.
Dance Princess
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macrophage69alpha said:
My blood sugar is low. My blood pressure is also consistently very low. The reason I thought it was electrolytes is because I heard it was a diuretic.
THANKS
macrophage69alpha
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increase your carbohydrate intake, eat more "slow carbs"
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