webby

Ive read on some peoples journals about legs coming in last but is there a general order in which the body looses fat? I carry most of my bodyfat around my mid section and very little on my arms.

trickymicky69

I would say its down to genetics but if I had to make an informed guess it would come off the face first, then the arms, legs, chest followed by the abdominal/oblique area.
Only from my experience though

YetiMan

Every one is different. Legs were my first thing to go along with bitch tits, then face and belly... Arms and back seemed last for me.

Flabby_Abbie

That's been my experience, too. I started on the Cambridge Diet at the beginning of last month (now maintaining at 8st 9) and I only had to lose half-a-stone to notice that my triple chin was now a single. I'm left with an 'apron' of loose skin round my abs, but I've been using Bio-Oil to tighten it, and it seems to be working.

Gone from 38-32-42 to 30-24-34 in six weeks (or a size 14-16 to a 6-8, depending on where I shop). Sorry, but I just love seeing the figures in black and white (not that I'm narcissistic or anything...)

I bought my first cami from Jane Norman the other day in a 'standard' 6 (JN stuff is sized a size smaller than everywhere else, so their 8s are 6s, 10s are 8s, etc.) Size 6 is a 30" bust, which is what this top measures as.

Sarah

Sarah

Macro

adiposity is related to both genes and hormones as well as environmental factors. Estrogen and Insulin play primary roles in reducing availability of stored fats (estrogen via upregulation of Alpha2 adrenoceptor- see article below and insulin via direct inhibition of lipolysis as well as adipogenesis-- thus the importance of maintaing good insulin sensitivity and blood glucose levels)

http://www.afboard.com/forum/anafit-...-estrogen.html

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Tatyana

More 'oestrogen is bad' internet rumour bull****e with no references.

It also doesn't consider leptin, ghrelin, peptide (sorry can't remember full name right now), dopamine reward system.

Sorry, not so simple, it is a case of someone taking one wee bit of physiology out of context.

The concept of eliminating oestrogen to increase fat loss is one of those bodybuilding myths, far too simplistic and simply outdated.

Gao Q, Horvath T. Crosstalk between estrogen and leptin signaling in the hypothalamus. Am J Physiol Endocrinol Metab. 2008 Mar 11 [Epub ahead of print]

Comparative Medicine, Yale University, New haven, Connecticut, United States.

Obesity, characterized by enhanced food intake (hyperphagia) and reduced energy expenditure that results in the accumulation of body fat, is a major risk factor for various diseases including diabetes, cardiovascular disease and cancer.

In the United States, more than half of adults are overweight and this number continues to increase (Flegal et al., 2002). The adipocyte secreted hormone, leptin, and its downstream signaling mediators play crucial roles in the regulation of energy balance.

Leptin decreases feeding while increasing energy expenditure and permitting energy-intensive neuroendocrine processes (such as reproduction). Thus, leptin also modulates the neuroendocrine reproductive axis.

The gonadal steroid hormone, estrogen, plays a central role in the regulation of reproduction and also contributes to the regulation of energy balance. Estrogen deficiency promotes feeding and weight gain, and estrogen facilitates and to some extent mimics some actions of leptin.

In this review, we examine the function of estrogen and leptin in the brain, with a focus on mechanisms by which leptin and estrogen cooperate in the regulation of energy homeostasis. Key words: estradiol, leptin, crosstalk.

Con

Every one is different generally women lose fat last on their legs but for me this is also the case legs and arms are the final place fat leaves while abbs are ripped long before they even start too look lean.

jodes

Girls point of view -For me, shoulders, arms, chest first, followed by abs, legs last.

Macro

you obviously dont understand this study or you would not have posted it. And certainly not highlighted that portion of the text. leptin insensitivity is linked to obesity, not low levels of leptin. Leptin levels in obese persons are actually generally very high. As are estrogen levels (due to aromatase). And to be clear there is a huge difference between hypoestrogenemic state (which is what that study refers to) and the hyperestrogenic being discussed in the article.

as to your criticism, the article does not say that estrogen is the cause of all adipose issues. What is says is that higher estrogen levels are linked to alpha2 proliferation (as well as female fat pattern and inhibition of lipolysis) and that aromatase increases due to fat gain increase levels of estrogen (primarily in men, but peripheral and local impacts of estrogen synthesis in women are also significant, highly linked to secondary conversion due to reduction of SHBG).

and because macro is nice and decidedly forgiving of your rudeness...

J Clin Endocrinol Metab. 2004 Apr;89(4):1869-78. Links

Estrogen controls lipolysis by up-regulating alpha2A-adrenergic receptors directly in human adipose tissue through the estrogen receptor alpha. Implications for the female fat distribution.

Pedersen SB, Kristensen K, Hermann PA, Katzenellenbogen JA, Richelsen B.
Department of Endocrinology and Metabolism, Aarhus Amtssygehus, Aarhus University Hospital, Denmark. sbp@dadlnet.dk
Estrogen seems to promote and maintain the typical female type of fat distribution that is characterized by accumulation of adipose tissue, especially in the sc fat depot, with only modest accumulation of adipose tissue intraabdominally. However, it is completely unknown how estrogen controls the fat accumulation. We studied the effects of estradiol in vivo and in vitro on human adipose tissue metabolism and found that estradiol directly increases the number of antilipolytic alpha2A-adrenergic receptors in sc adipocytes. The increased number of alpha2A-adrenergic receptors caused an attenuated lipolytic response of epinephrine in sc adipocytes; in contrast, no effect of estrogen on alpha2A-adrenergic receptor mRNA expression was observed in adipocytes from the intraabdominal fat depot. These findings show that estrogen lowers the lipolytic response in sc fat depot by increasing the number of antilipolytic alpha2A-adrenergic receptors, whereas estrogen seems not to affect lipolysis in adipocytes from the intraabdominal fat depot. Using estrogen receptor subtype-specific ligands, we found that this effect of estrogen was caused through the estrogen receptor subtype alpha. These findings demonstrate that estrogen attenuates the lipolytic response through up-regulation of the number of antilipolytic alpha2A-adrenergic receptors only in sc and not in visceral fat depots. Thus, our findings offer an explanation how estrogen maintains the typical female sc fat distribution because estrogen seems to inhibit lipolysis only in sc depots and thereby shifts the assimilation of fat from intraabdominal depots to sc depots.

1: J Lipid Res. 1999 Sep;40(9):1559-71. Links

Regional and gender variations in adipose tissue lipolysis in response to weight loss.

Mauriège P, Imbeault P, Langin D, Lacaille M, Alméras N, Tremblay A, Després JP.
Lipid Research Center, Laval University, Ste-Foy, Québec, Canada G1K 7P4.
Catecholamine-induced lipolysis was investigated in 32 obese subjects (14 men and 18 premenopausal women), aged 36-50 years, whose body mass index ranged from 30 to 42 kg/m(2). Isolated subcutaneous (subc) abdominal and femoral adipocytes were studied before and after a 15-week weight reducing program, during which mean body weight loss averaged 9 vs. 10 kg in women and men, respectively (P < 0.0001). Participants were re-examined when they were weight-stable. Fat cell weight decreased by about 15;-20% in both depots (P values ranging from 0.01 to 0.05). Epinephrine (mixed alpha2-/beta-adrenoceptor (AR) agonist) induced antilipolysis at low concentrations and a net lipolytic response at higher doses, irrespective of subjects' fatness and anatomic location of fat. Basal lipolysis, maximal lipolytic responses to isoprenaline (beta-AR agonist), dobutamine and procaterol (beta1- and beta2-AR agonists, respectively) as well as maximal antilipolytic effects of epinephrine or UK-14304 (alpha2-AR agonist) were similar before and after weight reduction. However, both beta- and beta2-AR lipolytic sensitivities and the beta-AR density were increased in both genders after weight reduction, this effect being more marked in subc abdominal than in femoral adipocytes (P values ranging from 0.001 to 0.05). The alpha2-AR antilipolytic sensitivity was reduced in adipose cells from both regions in women, but only in subc abdominal adipocytes in men (P < 0.05), although the alpha2-AR density remained unchanged after weight reduction. In conclusion, a moderate weight loss leads to a higher adipose cell lipolytic efficiency which is associated with changes at receptor levels (mainly an increased beta2- and a decreased alpha2-AR sensitivities), in both genders.

1: Int J Obes Relat Metab Disord. 1997 Apr;21(4):314-20. Links

Lipolytic catecholamine resistance linked to alpha 2-adrenoceptor sensitivity--a metabolic predictor of weight loss in obese subjects.

Hellström L, Rössner S, Hagström-Toft E, Reynisdottir S.
Department of Medicine, Karolinska Institute, Huddinge University Hospital, Sweden.
OBJECTIVE: The weight loss achieved during treatment with very-low-calorie diets (VLCD) varies between individuals. The aim of this study was to investigate whether interindividual variations in catecholamine-induced lipolysis are of importance for the rate of weight loss during VLCD. DESIGN: Prospective study. SUBJECTS: Twenty-eight obese, but otherwise healthy and drug-free women aged 20-57 y with BMI 33.3-47.5 kg/m2 were investigated before entering a four week weight reduction program with a calorie-restricted diet. MEASUREMENTS: A subcutaneous adipose tissue biopsy was obtained from the abdominal area. Isolated fat cells were prepared and incubated in vitro with agents acting on lipolysis at defined steps in the lipolytic cascade. Glycerol release was measured and used as a lipolytic index. Following the biopsy, the subjects underwent a four week VLCD treatment. RESULTS: The decrease in body weight in the whole group ranged between 4.8 and 13.5 kg. Dietary compliance was ascertained by daily measurements of urine-ketones and regular interviews and was satisfactory in all subjects throughout the study. Based on percent body weight reduction, the material was divided into two equally sized groups, classified as rapid or slow weight losers. The rapid weight losers were 10-fold more sensitive to the lipolytic effect of noradrenaline (P = 0.04) and 10-fold less sensitive (P = 0.002) to the antilipolytic effect induced by the alpha 2-adrenoceptor agonist clonidine than the slow weight losers. In the whole material, weight loss was significantly correlated (adjusted r2 = 0.25) with alpha 2-adrenoceptor sensitivity. CONCLUSION: Rapid weight loss during VLCD is associated with increased adipocyte lipolytic sensitivity to catecholamines due to decreased alpha 2-adrenoceptor sensitivity, which in turn may promote lipid mobilization. It appears that variations in alpha 2-adrenoceptor sensitivity in adipocytes may be predictive of weight loss during VLCD.

1: Clin Endocrinol (Oxf). 2007 Mar;66(3):440-6. Links

Intra-adipose sex steroid metabolism and body fat distribution in idiopathic human obesity.

Wake DJ, Strand M, Rask E, Westerbacka J, Livingstone DE, Soderberg S, Andrew R, Yki-Jarvinen H, Olsson T, Walker BR.
Endocrinology Unit, Centre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, Scotland, UK.
OBJECTIVE: Causes of visceral fat accumulation include glucocorticoid excess or decreased oestrogen/androgen ratio either in plasma or within adipose tissue. In obese subjects, the intra-adipose cortisol-generating enzyme 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) is increased, but information on sex steroid signalling is sp****. We aimed to test associations between body fat or fat distribution and mRNA transcript levels for androgen and oestrogen receptors and for enzymes metabolizing sex steroids in adipose tissue. DESIGN: A cross-sectional study. PATIENTS: Forty-five healthy men and women with body mass index (BMI) 21-36 kg/m(2). MEASUREMENTS: In subcutaneous adipose biopsies we measured mRNAs for enzymes metabolizing local oestrogens (aromatase) and androgens [5alpha-reductase type 1; AKR1C2 (3alpha-HSD3); AKR1C3 (17beta-HSD5, 3alpha-HSD2)] and for sex steroid receptors [oestrogen receptor (ER)-alpha and androgen receptor (AR)]. We related these to body fat mass and distribution. RESULTS: Generalized obesity (BMI) was associated with increased aromatase mRNA (r = 0.35, P < 0.05). Central obesity (waist : hip ratio) was associated with mRNA for AKR1C2 (r = 0.28, P < 0.05) and AKR1C3 (r = 0.38, P < 0.01) but not aromatase (r = 0.06). 5alpha-Reductase type 1, ER and AR mRNA levels did not predict fat amount or its distribution. CONCLUSION: These data on transcript levels suggest that, in idiopathic obesity, increased intra-adipose oestrogen generation by aromatase predicts peripheral fat distribution, while androgen metabolism by AKR1C isoforms predicts central fat distribution, supporting the hypothesis that intra-adipose sex steroid metabolism is a determinant of gynoid vs. android patterns of body fat.

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Gains

I'm in the process of getting lean at the moment, and so far it's been back, arms, face, legs and finally abs/midsection. I can see I'm going to be one of those blokes who only has visible abs when very lean, unlike Con you lucky b@stard

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Macro

1: Metabolism. 1998 Apr;47(4):467-73. Links
Regional differences in adrenoceptor binding and fat cell lipolysis in obese, postmenopausal women.Berman DM, Nicklas BJ, Rogus EM, Dennis KE, Goldberg AP.
Department of Medicine, University of Maryland School of Medicine; the Geriatric Research, Education and Clinical Center, Baltimore Veterans Affair Medical Center, 21201, USA.

In women there is an increase in visceral obesity, subcutaneous abdominal adipocyte lipolysis, and risk of cardiovascular disease (CVD) associated with weight gain after menopause. The mechanisms underlying this increase in adrenoreceptor (AR)-agonist catecholamine-stimulated lipolysis and abdominal obesity in postmenopausal women were studied in intact adipocytes isolated from the abdominal and gluteal subcutaneous fat depots in 19 obese (48% +/- 1% body fat, mean +/- SE) women with a mean +/- SE age of 58 +/- 1 years. The fat cell size and adipose tissue lipoprotein lipase (ATLPL) activity were similar in both sites. The maximal lipolytic responsiveness and sensitivity to isoproterenol were higher (P < .05) in abdominal compared with gluteal adipocytes, but maximal lipolytic response to a post-AR agent was similar. Abdominal adipocytes had a higher beta-AR ([3H]-CGP-12177) and alpha2-AR ([3H]-yohimbine) affinity than gluteal cells (P < .05), lower alpha2-AR density (P < .05), but similar beta-AR density as gluteal cells. Both abdominal and gluteal cell size correlated with alpha2-AR density (P < .01), but not with beta-AR density. Thus, a higher beta-AR affinity and lower alpha2-AR relative to beta-AR density may explain the higher in vitro catecholamine-mediated lipolysis in abdominal compared with gluteal adipocytes in obese, postmenopausal women.


1: Cell Mol Life Sci. 2003 Sep;60(9):1982-9. Links
Gender- and site-related effects on lipolytic capacity of rat white adipose tissue.Pujol E, Rodríguez-Cuenca S, Frontera M, Justo R, Lladó I, Kraemer FB, Gianotti M, Roca P.
Grup de metabolisme energètic i nutrició, Departament de Biologia Fonamental i Ciències de la Salut, Universitat de les Illes Balears, Cra. Valldemossa km 7.5, 07122 Palma de Mallorca, Spain.

Gender- and site-related differences in the lipolytic capacity, at the different steps of the adrenergic pathway, in gonadal and inguinal white adipose tissue (WAT), were assessed by studying alpha2A-adrenergic receptor (AR), beta3-AR and hormone-sensitive lipase (HSL) protein levels, and by determining the lipolytic response to different agents. Gonadal WAT showed a lower alpha2A/beta3-AR ratio, a greater lipolytic capacity in response to AR agonists, and higher HSL activity and protein levels than inguinal WAT. In female rats, we found greater alpha2A-AR protein levels and alpha2A/beta3-AR ratio compared to their male counterparts, but, on the other hand, a higher lipolytic response to beta-AR agonists and a greater lipolytic capacity at the postreceptor level, including a more activated HSL protein. Thus, the lipolytic capacity was clearly higher in gonadal than in inguinal WAT, at the different steps of the adrenergic pathway studied. Moreover, in both tissues, females showed a greater inhibition of lipolysis via alpha2-AR, which was counteracted by the higher lipolytic capacity at the postreceptor level.

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hackskii

I always suspected excess estrogen to play a part in bellyfat in men.
Excess aromatase effects testosterone production too.

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Macro

with respect to soft belly fat, yes. the intra-abdominal fat is due more to androgenic and insulin influence (gut and belly distention)

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