scholarly journals The effect of intermittent energy and carbohydrate restrictionv. daily energy restriction on weight loss and metabolic disease risk markers in overweight women

2013 ◽  
Vol 110 (8) ◽  
pp. 1534-1547 ◽  
Author(s):  
Michelle Harvie ◽  
Claire Wright ◽  
Mary Pegington ◽  
Debbie McMullan ◽  
Ellen Mitchell ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Weight Loss ◽  
Insulin Sensitivity ◽  
Body Fat ◽  
Disease Risk ◽  
Phase 1 ◽  
Weight Maintenance ◽  
Energy Restriction ◽  
Overweight Women ◽  
Daily Energy

Intermittent energy restriction may result in greater improvements in insulin sensitivity and weight control than daily energy restriction (DER). We tested two intermittent energy and carbohydrate restriction (IECR) regimens, including one which allowedad libitumprotein and fat (IECR+PF). Overweight women (n115) aged 20 and 69 years with a family history of breast cancer were randomised to an overall 25 % energy restriction, either as an IECR (2500–2717 kJ/d, < 40 g carbohydrate/d for 2 d/week) or a 25 % DER (approximately 6000 kJ/d for 7 d/week) or an IECR+PF for a 3-month weight-loss period and 1 month of weight maintenance (IECR or IECR+PF for 1 d/week). Insulin resistance reduced with the IECR diets (mean − 0·34 (95 % CI − 0·66, − 0·02) units) and the IECR+PF diet (mean − 0·38 (95 % CI − 0·75, − 0·01) units). Reductions with the IECR diets were significantly greater compared with the DER diet (mean 0·2 (95 % CI − 0·19, 0·66) μU/unit,P= 0·02). Both IECR groups had greater reductions in body fat compared with the DER group (IECR: mean − 3·7 (95 % CI − 2·5, − 4·9) kg,P= 0·007; IECR+PF: mean − 3·7 (95 % CI − 2·8, − 4·7) kg,P= 0·019; DER: mean − 2·0 (95 % CI − 1·0, 3·0) kg). During the weight maintenance phase, 1 d of IECR or IECR+PF per week maintained the reductions in insulin resistance and weight. In the short term, IECR is superior to DER with respect to improved insulin sensitivity and body fat reduction. Longer-term studies into the safety and effectiveness of IECR diets are warranted.

scholarly journals Dietary Composition in Restoring Reproductive and Metabolic Physiology in Overweight Women with Polycystic Ovary Syndrome

2003 ◽  
Vol 88 (2) ◽  
pp. 812-819 ◽  
Author(s):  
L. J. Moran ◽  
M. Noakes ◽  
P. M. Clifton ◽  
L. Tomlinson ◽  
R. J. Norman
Keyword(s):  
Insulin Resistance ◽  
Weight Loss ◽  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Weight Maintenance ◽  
Density Lipoprotein ◽  
Energy Restriction ◽  
Ovary Syndrome ◽  
Overweight Women ◽  
Free Androgen Index

Overweight women with polycystic ovary syndrome (PCOS) were randomized to a high protein (HP; 40% carbohydrate and 30% protein; n = 14) or a low protein (LP; 55% carbohydrate and 15% protein) diet (n = 14). The intervention consisted of 12 wk of energy restriction (∼6000 kJ/d), followed by 4 wk of weight maintenance. Pregnancies (two HP and one LP); improvements in menstrual cyclicity, lipid profile, and insulin resistance (as measured by the homeostasis model); and decreases in weight (7.5%) and abdominal fat (12.5%) occurred independently of diet composition. Improvements in menstrual cyclicity were associated with greater decreases in insulin resistance and fasting insulin (P = 0.011). On the LP diet, high density lipoprotein cholesterol decreased 10% during energy restriction (P = 0.008), and the free androgen index increased 44% in weight maintenance stages (P = 0.027). Weight loss leads to improvements in cardiovascular and reproductive parameters potentially mediated by improvements in surrogate measures of insulin resistance. An HP weight loss diet may result in minor differential endocrine and metabolic improvements.

scholarly journals Differential Trajectories in Altered Insulin Sensitivity Following Weight Loss and Their Impact on Circulatory Amino Acids: Results from the PREVIEW: New Zealand Sub-study (OR27-07-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Utpal Prodhan ◽  
Amber Milan ◽  
Marta Silvestre ◽  
Pia Christensen ◽  
Anne Raben ◽  
...  
Keyword(s):  
Amino Acids ◽  
Weight Loss ◽  
New Zealand ◽  
Insulin Sensitivity ◽  
Disease Risk ◽  
Energy Restriction ◽  
Investment Fund ◽  
Funding Sources ◽  
Dietary Energy Restriction ◽  
Seed Funding

Abstract Objectives Metabolite profiling studies have consistently identified altered circulatory concentrations of amino acids (AAs) in individuals with heightened risk of type 2 diabetes and cardiovascular diseases. Of the changes reported to date, the branched-chain amino acids (BCAA) may be a reliable biomarker of disease risk and have been reported to be elevated many years prior to the onset of diabetes. We hypothesised that energy restriction-associated weight loss in pre-diabetes individuals would result in altered profile of circulatory AAs, including BCAA, with the changes correlating with the improvement in insulin sensitivity. Methods Pre-diabetic individuals (confirmed using the American Diabetes Association criteria) aged 25–70 years with BMI > 25 kg/m2 recruited into the New Zealand arm of the PREVIEW diabetes prevention trial, participated in an 8-week weight reduction program, with a requirement to lose ≥ 8% initial body weight using a commercial low-calorie diet (LCD, Cambridge Diet, UKTM). Among those who succeeded, current analysis based on available samples (n = 168) from baseline (week-0) and end of weight loss (week-8). Serum free AA concentrations measured by ultra-high pressure liquid chromatography (UPLC) and all other metabolites measured using standard assays. Results Significant weight loss (11.1 ± 0.2% from baseline) accompanied improved insulin sensitivity and lipid profile. BCAA concentration positively correlated with insulin resistance measured at week 0 and 8, correspondingly (P < 0.05). Although the concentration of some AAs reduced significantly from week 0 to 8 (P < 0.05), reduction in fasting BCAA concentration was not significant (P > 0.05). However, regression analysis demonstrated that independent of weight loss, every 1.0 standard deviation (SD) reduction in BCAA concentration was associated with improvement in insulin sensitivity by 1.9 SD (P < 0.05). Conclusions As expected, dietary energy restriction-associated weight loss in individuals with pre-diabetes contributes towards normalisation of insulin sensitivity. Further, the responsiveness of AA and BCAA profiles to weight loss may be beneficial for monitoring and overseeing disease risk and improvement. Funding Sources This research was funded by the EU 7th Framework Programme; the New Zealand Health Research Council; the Food and Health Programme Seed Funding, University of Auckland; and AgResearch Limited (the Strategic Science Investment Fund). Cambridge Weight Plan, Ltd, UKTM provided the commercial LCD.

scholarly journals In Vivo Changes in Central and Peripheral Insulin Sensitivity in a Large Animal Model of Obesity

Endocrinology ◽  
2012 ◽  
Vol 153 (7) ◽  
pp. 3147-3157 ◽  
Author(s):  
Clare L. Adam ◽  
Patricia A. Findlay ◽  
Raymond P. Aitken ◽  
John S. Milne ◽  
Jacqueline M. Wallace
Keyword(s):  
Insulin Resistance ◽  
Weight Loss ◽  
Insulin Sensitivity ◽  
Body Fat ◽  
Plasma Insulin ◽  
Area Under The Curve ◽  
Tolerance Test ◽  
Blood Brain ◽  
Ad Libitum

Obesity disrupts homeostatic energy balance circuits leading to insulin resistance. Here we examined in vivo peripheral and central insulin sensitivity, and whether central insensitivity in terms of the voluntary food intake (VFI) response occurs within the hypothalamus or at blood-brain transfer level, during obesity and after subsequent weight loss. Sheep with intracerebroventricular (icv) cannulae were fed complete diet for 40 wk ad libitum (obese group) or at control level (controls). Thereafter, obese sheep were food restricted (slimmers) and controls fed ad libitum (fatteners) for 16 wk. Dual-energy x-ray absorptiometry (DEXA) measured total body fat, insulin analyses in blood and cerebrospinal fluid (CSF) assessed blood-brain transfer, iv glucose tolerance test (GTT) and insulin tolerance test (ITT) measured peripheral insulin sensitivity, and VFI responses to icv insulin assessed intrahypothalamic sensitivity. Insulinemia was higher in obese than controls; plasma insulin correlated with DEXA body fat and CSF insulin. Insulinemia was higher in fatteners than slimmers but ratio of CSF to plasma insulin correlated only in fatteners. Plasma glucose baseline and area under the curve were higher during GTT and ITT in obese than controls and during ITT in fatteners than slimmers. GTT and ITT glucose area under the curve correlated with DEXA body fat. VFI decreased after icv insulin, with response magnitude correlating negatively with DEXA body fat. Overall, insulin resistance developed first in the periphery and then within the brain, thereafter correlating with adiposity; central resistance in terms of VFI response resulted from intrahypothalamic insensitivity rather than impaired blood-brain transfer; modest weight loss improved peripheral but not central insulin sensitivity and induced central hypoinsulinemia.

Abstract P250: Insulin Resistance During Pregnancy is Inversely Associated With Gynoid Fat Distribution Postpartum

Circulation ◽  
2018 ◽  
Vol 137 (suppl_1) ◽  
Author(s):  
Katherine H Ingram ◽  
Roxanna Lopez
Keyword(s):  
Insulin Resistance ◽  
Weight Gain ◽  
Insulin Sensitivity ◽  
Gestational Weight Gain ◽  
Body Fat ◽  
Visceral Fat ◽  
Post Partum ◽  
Lower Body ◽  
Negatively Associated ◽  
Gestational Weight

An association between abdominal adiposity and insulin resistance is well-established. Recent research indicates that subcutaneous fat accumulation in the lower body may be associated with higher levels of insulin sensitivity. Hypothesis: This pilot study tested the hypothesis that the distribution of body fat in the lower body after pregnancy is negatively associated with gestational insulin resistance. Methods: In 32 nulliparous pregnant women (age 27±4.5, BMI 29.5±7.9, 69% non-hispanic white), the Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) was computed from fasting glucose and insulin at 24-28 weeks gestation. Body composition was assessed at mid-gestation (18-20 weeks) and at four weeks post-partum. Total body fat was estimated via bioelectrical impedance (InBody 720) and skinfold thicknesses were measured at seven sites. Dual-energy xray absorptiometry (DXA) measures of regional fat (gynoid, visceral, and leg) were obtained post-partum only. Gestational weight gain was monitored by medical records. Partial correlation analyses were controlled for age and race and then analyses were repeated controlling for baseline (mid-gestation) body fat percent. HOMA-IR was log-transformed for normality. Results: HOMA-IR was associated with post-partum body fat ( r =0.45, p < .05) and adiposity in the trunk region ( r =0.58, 0.57 and 0.52 for DXA visceral fat, suprailiac skinfold, and abdominal skinfold, respectively, p < .01), but not with gestational weight gain ( r =.07, p = ns), DXA gynoid region ( r = 0.26, p = ns), or any other leg measure. When analyses were further controlled for baseline body fat, post-partum measures of lower-body adiposity were strongly and negatively correlated with HOMA-IR ( r = -0.66, -0.48, and -0.48 for thigh skinfold, DXA gynoid, and DXA leg, respectively, p < .05 for all). Neither DXA visceral fat ( r = .23; p = ns) nor any other post-partum fat measures were associated with HOMA-IR when controlling for baseline body fat. Conclusions: Gestational insulin resistance was negatively associated with post-partum thigh fat accumulation, independent of overall body fat. These data indicate that insulin sensitivity may be associated with the ability to store fat in the lower body and should warrant further study of subcutaneous leg fat as a metabolically “healthy” storage depot.

scholarly journals Hyperandrogenism and Insulin Resistance, Not Changes in Body Weight, Mediate the Development of Endothelial Dysfunction in a Female Rat Model of Polycystic Ovary Syndrome (PCOS)

Endocrinology ◽  
2015 ◽  
Vol 156 (11) ◽  
pp. 4071-4080 ◽  
Author(s):  
Amanda Hurliman ◽  
Jennifer Keller Brown ◽  
Nicole Maille ◽  
Maurizio Mandala ◽  
Peter Casson ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Weight Gain ◽  
Insulin Sensitivity ◽  
Endothelial Dysfunction ◽  
Polycystic Ovary Syndrome ◽  
Rat Model ◽  
Polycystic Ovary ◽  
Phase 1 ◽  
Ovary Syndrome

This study was designed to differentiate the contributions of hyperandrogenism, insulin resistance (IR), and body weight to the development of endothelial dysfunction in polycystic ovary syndrome and determine the effectiveness of insulin sensitization and antiandrogenic therapy after the establishment of vascular and metabolic dysfunction using a rat model of polycystic ovary syndrome. We hypothesized that the observed endothelial dysfunction was a direct steroidal effect, as opposed to changes in insulin sensitivity or body weight. Prepubertal female rats were randomized to the implantation of a pellet containing DHT or sham procedure. In phase 1, DHT-exposed animals were randomized to pair feeding to prevent weight gain or metformin, an insulin-sensitizing agent, from 5 to 14 weeks. In phase 2, DHT-exposed animals were randomized to treatment with metformin or flutamide, a nonsteroidal androgen receptor blocker from 12 to 16 weeks. Endothelial function was assessed by the vasodilatory response of preconstricted arteries to acetylcholine. Serum steroid levels were analyzed in phase 1 animals. Fasting blood glucose and plasma insulin were analyzed and homeostasis model assessment index calculated in all animals. Our data confirm the presence of endothelial dysfunction as well as increased body weight, hypertension, hyperinsulinemia, and greater IR among DHT-treated animals. Even when normal weight was maintained through pair feeding, endothelial dysfunction, hyperinsulinemia, and IR still developed. Furthermore, despite weight gain, treatment with metformin and flutamide improved insulin sensitivity and blood pressure and restored normal endothelial function. Therefore, the observed endothelial dysfunction is most likely a direct result of hyperandrogenism-induced reductions in insulin sensitivity, as opposed to weight gain.

scholarly journals Pioglitazone improves insulin resistance and decreases blood pressure in adult patients with congenital adrenal hyperplasia

2009 ◽  
Vol 161 (6) ◽  
pp. 887-894 ◽  
Author(s):  
Jeanne Margot Kroese ◽  
Christiaan F Mooij ◽  
Marinette van der Graaf ◽  
Ad R M M Hermus ◽  
Cees J Tack
Keyword(s):  
Insulin Resistance ◽  
Blood Pressure ◽  
Insulin Sensitivity ◽  
Body Fat ◽  
Matched Control ◽  
Fat Distribution ◽  
Body Fat Distribution ◽  
Adrenal Hyperplasia ◽  
Insulin Resistant ◽  
Steroid Profiles

ContextPatients with congenital adrenal hyperplasia (CAH) are chronically treated with supraphysiological doses of glucocorticoids, which are known to induce insulin resistance. Thiazolidinediones might reverse this effect and improve insulin sensitivity.ObjectivesTo assess insulin sensitivity in CAH patients and the effect of pioglitazone treatment on insulin sensitivity in CAH patients. Secondary objectives were the effects of treatment with pioglitazone on blood pressure, body fat distribution, lipid, and steroid profiles.DesignRandomized placebo controlled crossover trial.ParticipantsTwelve CAH patients and 12 body mass and age-matched control subjects.InterventionSixteen-week treatment with pioglitazone (45 mg/day) or placebo.Main outcome measureInsulin sensitivity measured by euglycemic clamp and oral glucose tolerance test. Further measures were 24-h blood pressure profiles, body fat distribution measured by magnetic resonance imaging, dual energy x-ray absorptiometry (DEXA) and bioimpedance procedures, liver fat by magnetic resonance spectroscopy, lipid, and steroid profiles.ResultsCAH patients were insulin resistant compared with healthy controls. Treatment with pioglitazone significantly improved insulin sensitivity in CAH patients (glucose infusion rate (GIR) from 28.5±11.6 to 38.9±11.0 μmol/kg per min, P=0.000, GIR in controls 46.2±23.4 μmol/kg per min, P<0.05 versus CAH). Treatment with pioglitazone decreased blood pressure (systolic: 124.0±13.6 vs 127.0±14.9 mmHg, P<0.001, diastolic: 72.8±11.5 vs 77.4±12.6 mmHg, P<0.001). No changes in body fat distribution, lipid, and steroid profiles were observed.ConclusionsCAH patients are insulin resistant compared with matched control subjects. Treatment with pioglitazone improves insulin sensitivity and decreases blood pressure in CAH patients.

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