***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Short term fasting activates the corticotropic and somatotropic , and suppresses the reproductive , axis in men . Analogous neuroendocrine responses are less well characterized in women . Recently , we identified a negative association between the adipocyte-derived nutritional signaling peptide , leptin , and pulsatile GH secretion in older fed women . In the present study , we investigated the impact of acute nutrient deprivation on pulsatile GH and LH secretion and mean leptin concentrations in eight healthy young women in the sex-steroid replete milieu of the midluteal phase of the normal menstrual cycle . Volunteers underwent 24-h blood sampling during r and omly ordered , short term ( 2.5-day ) , fasting vs. fed sessions in separate menstrual cycles . Pulsatile GH and LH secretion over 24 h was quantified by deconvolution analysis , nyctohemeral rhythmicity was quantified by cosinor analysis , and the orderliness of the GH or LH release process was quantified by the approximate entropy statistic . By paired statistical analysis , a 2.5-day fast failed to alter mean ( pooled ) 24-h serum concentrations of LH , progesterone , estradiol , or PRL , but increased cortisol levels more than 1.5-fold ( P = 0.0003 ) . Concurrently , mean ( pooled ) serum leptin concentrations fell by 75 % ( P = 0.0003 ) , and insulin-like growth factor I ( IGF-I ; P < 0.05 ) and insulin decreased significantly ( P = 0.0018 ) . In contrast , the daily pulsatile GH secretion rate rose 3-fold ( P < 0.001 ) . Amplified daily GH secretion was attributable mechanistically to a 2.3-fold rise in GH secretory burst mass , reflecting an increased GH secretory burst amplitude ( P < 0.01 ) . The GH half-life , duration of GH secretory bursts , and GH pulse frequency did not vary during short term fasting . The disorderliness of GH release increased significantly with nutrient restriction ( P = 0.005 ) . The mesor and amplitude of the nyctohemeral serum GH concentration rhythm also rose with fasting ( P < 0.01 ) , but the timing of maximal serum GH concentrations did not change . Thus , short-term ( 2.5-day ) fasting during the sex steroid-replete midluteal phase of the menstrual cycle in healthy young women profoundly suppresses 24-h serum leptin and insulin ( and to a lesser degree , IGF-I ) concentrations , augments cortisol release , but fails to alter daily LH , estradiol , or progesterone concentrations . In contrast , the GH axis exhibits strikingly amplified pulsatile secretion , increased nyctohemeral rhythmicity , and marked disorderliness of the release process . We conclude that the somatotropic axis is more evidently vulnerable to short-term nutrient restriction than the reproductive axis in steroidogenically sufficient midluteal phase women . This study invites the question of whether normal ( nutritionally replete ) GH secretory dynamics can be restored in fasting women by human leptin , insulin , or IGF-I infusions BACKGROUND Weight loss , through calorie restriction or increases in energy expenditure via exercise , improves glucose tolerance and insulin action . However , exercise-induced energy expenditure may further improve glucoregulation through mechanisms independent of weight loss . OBJECTIVE The objective was to assess the hypothesis that weight loss through exercise-induced energy expenditure improves glucoregulation and circulating factors involved in insulin action to a greater extent than does similar weight loss through calorie restriction . DESIGN Sedentary men and women aged 50 - 60 y with a body mass index ( kg/m(2 ) ) of 23.5 - 29.9 were r and omly assigned to 1 of 2 weight-loss interventions [ 12 mo of exercise training ( EX group ; n = 18 ) or calorie restriction ( CR group ; n = 18 ) ] or to a healthy lifestyle ( HL ) control group ( n = 10 ) . The insulin sensitivity index and areas under the curve for glucose and insulin were assessed with an oral-glucose-tolerance test . Adiponectin and tumor necrosis factor alpha concentrations were measured in fasting serum . Fat mass was measured by dual-energy X-ray absorptiometry . RESULTS Yearlong energy deficits were not significantly different between the EX and CR groups , as evidence d by body weight and fat mass changes . The insulin sensitivity index increased and the glucose and insulin areas under the curve decreased in the EX and CR groups , remained unchanged in the HL group , and did not differ significantly between the EX and CR groups . Marginally significant increases in adiponectin and decreases in the ratio of tumor necrosis factor alpha to adiponectin occurred in the EX and CR groups but not in the HL group . CONCLUSIONS Weight loss induced by exercise training or calorie restriction improves glucose tolerance and insulin action in nonobese , healthy , middle-aged men and women . However , it does not appear that exercise training-induced  weight loss results in greater improvements than those that result from calorie restriction alone Using a double-blind , placebo-controlled crossover design , the effects of 48 h near complete energy restriction on endocrine regulators of appetite and satiety were assessed . Twelve men and one woman participated in this controlled , 2-day diet intervention study . One experimental trial was completed in a calorie deprived state ( CAL-DEP ; < 10 % of estimated energy requirements ) and others in a fed condition ( carbohydrate only and carbohydrate and fat ; data were pooled and compared to CAL-DEP ) . Test meals containing prescribed energy intake and indistinguishable in sensory characteristics were provided during each trial . Glucose , insulin , leptin , ghrelin , cortisol , dehydroepi and rosterone-sulfate ( DHEA-S ) , and satiety were repeatedly assessed . Mean glucose , insulin , and leptin concentrations were lower ( P < 0.0001 ) for CAL-DEP compared to the fully fed ( FED ) state . Ghrelin and DHEA-S were higher ( P < 0.0001 ) for CAL-DEP relative to FED . Cortisol levels declined each day regardless of diet ( P < 0.0001 ) but were 32 % higher ( P < 0.01 ) at the conclusion of the session for CAL-DEP compared to FED . Satiety was 25 % lower ( P < 0.0001 ) for CAL-DEP relative to FED and decreased ( P < 0.0001 ) over time regardless of diet . In the FED state , insulin ( r = 0.55 ) , glucose ( r = 0.76 ) , cortisol ( r = -0.59 ) , and DHEA-S ( r = -0.62 ) were associated ( P < 0.05 ) with satiety , but not during CAL-DEP . These findings show that 2 days of severe energy restriction alter several endocrine regulators of appetite independent of perception of increased hunger suggesting a physiological mechanism to explain overeating following acute periods of severe energy restriction Controversy exists as to whether endogenous cortisol production is associated with visceral obesity and insulin resistance in humans . We therefore quantified cortisol production and clearance rates , abdominal fat depots , insulin sensitivity , and adipocyte gene expression in a cohort of 24 men . To test whether the relationships found are a consequence rather than a cause of obesity , eight men from this larger group were studied before and after weight loss .  Daily cortisol production rates ( CPR ) , free cortisol levels ( FC ) , and metabolic clearance rates ( MCR ) were measured by stable isotope methodology and 24-h sampling ; intra-abdominal fat ( IAF ) and subcutaneous fat ( SQF ) by computed tomography ; insulin sensitivity ( S(I ) ) by frequently sample d intravenous glucose tolerance test ; and adipocyte 11beta-hydroxysteroid dehydrogenase-1 ( 11beta-HSD-1 ) gene expression by quantitative RT-PCR from subcutaneous biopsies . Increased CPR and FC correlated with increased IAF , but not SQF , and with decreased S(I ) . Increased 11beta-HSD-1 gene expression correlated with both IAF and SQF and with decreased S(I ) . With weight loss , CPR , FC , and MCR did not change compared with baseline ; however , with greater loss in body fat than lean mass during weight loss , both CPR and FC increased proportionally to final fat mass and IAF and 11beta-HSD-1 decreased compared with baseline . These data support a model in which increased hypothalamic-pituitary-adrenal activity in men promotes selective visceral fat accumulation and insulin resistance and may promote weight regain after diet-induced weight loss , whereas 11beta-HSD-1 gene expression in SQF is a consequence rather than cause of adiposity We have previously described that serum corticosteroid binding globulin ( CBG ) concentrations are associated with insulin secretion . The present study was design ed to evaluate the effects of changing insulin concentrations , both endogenous and after exogenous insulin administration , on circulating CBG levels in vivo . Serum CBG concentrations were measured during an insulin-modified frequently sample d intravenous ( IV ) glucose tolerance test ( FSIVGT ) in 14 lean and 19 obese otherwise healthy subjects with varying degrees of glucose tolerance .  Acute insulin response to glucose ( AIRg ) correlated significantly with serum CBG concentrations at time 0 ( r = -.38 , P = .029 ) , 22 minutes ( r = -.41 , P = .01 ) , 50 minutes ( r = -.41 , P = .01 ) , and 180 minutes ( r = -.39 , P = .02 ) . Insulin sensitivity ( S(I ) ) was not associated with serum CBG concentration at time 0 ( r = -.16 , P = not significant [ NS ] ) , but correlated significantly with CBG concentration at 22 minutes ( r = -.41 , P = .02 ) and 50 minutes ( r = -.35 , P = .048 ) of the FSIVGT . In lean subjects , serum CBG concentration decreased significantly after IV insulin from 37.9 + /- 5.4 to 35.4 + /- 3 mg/L ( P = .02 ) and returned to basal levels thereafter . In contrast , obese , glucose-tolerant subjects had lower CBG levels than lean and obese glucose intolerant subjects ( 33.8 + /- 3.0 v 37.9 + /- 5.4 and 39.8 + /- 4.4 mg/L , respectively ) , and their serum CBG concentrations remained unchanged during FSIVGT . Mean serum-free insulin-like growth factor-I ( IGF-I ) concentrations steadily declined from 1.21 + /- 0.81 to 0.8 + /- 0.36 microg/L during the FSIVGT , and this effect was restricted to lean subjects . Basal serum-free IGF-I did not correlate with CBG levels at time 0 , but correlated inversely with the serum CBG concentrations at 22 minutes ( r = -.36 , P = .04 ) . Stepwise multivariant analysis showed that AIRg ( P = .035 ) and S(I ) ( P = .046 ) , but not free IGF-I levels , independently contributed to 28 % of CBG variance at 22 minutes . These results suggest that insulin , but not IGF-I , constitutes an important negative regulator of CBG liver synthesis . Endogenous and exogenous insulin do not affect serum CBG concentrations in insulin-resistant obese subjects with preserved or decreased insulin secretion . Obese glucose-tolerant subjects are hypothesized to exhibit tonically inhibited serum CBG levels . In contrast , in lean subjects , the higher the insulin secretion the lower the serum CBG concentration . The mechanisms of this CBG inhibitory effect exerted by insulin and its implication on cortisol homeostasis and fat distribution in humans await further investigations Objective : To test the hypothesis that dieting , or the restriction of caloric intake , is ineffective because it increases chronic psychological stress and cortisol production — two factors that are known to cause weight gain ; and to examine the respective roles of the two main behaviors that comprise dieting — monitoring one 's caloric intake and restricting one 's caloric intake — on psychological and biological stress indicators . Methods : In a 2 ( monitoring vs. not ) × 2 ( restricting vs. not ) fully crossed , controlled experiment , 121 female participants were assigned r and omly to one of four dietary interventions for 3 weeks . The monitoring + restricting condition tracked their caloric intake and restricted their caloric intake ( 1200 kcal/day ) ; the monitoring only condition tracked their caloric intake but ate normally ; the restricting only condition was provided 1200 kcal/day of food but did not track their calories , and the control group ate normally and did not track their intake . Before and after the interventions , participants completed measures of perceived stress and 2 days of diurnal saliva sampling to test for cortisol . Results : Restricting calories increased the 
    Output:
    
These results suggest that severe caloric restriction causes activation of the hypothalamic-pituitary-adrenal axis , which may be transient , but results in elevated cortisol which could mediate effects of starvation on brain and metabolic function as well as ameliorate weight loss