scholarly journals Reply to Landry et al. Findings from Diet Comparison Difficult to Interpret in the Absence of Adherence Assessment. Comment on “Tricò et al. Effects of Low-Carbohydrate versus Mediterranean Diets on Weight Loss, Glucose Metabolism, Insulin Kinetics and β-Cell Function in Morbidly Obese Individuals. Nutrients 2021, 13, 1345”

Nutrients ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 3695
Author(s):  
Domenico Tricò ◽  
Diego Moriconi ◽  
Monica Nannipieri
Keyword(s):  
Weight Loss ◽  
Glucose Metabolism ◽  
Cell Function ◽  
Morbidly Obese ◽  
Β Cell ◽  
Insulin Kinetics ◽  
Adherence Assessment ◽  
Low Carbohydrate ◽  
Β Cell Function

We thank Dr. Landry and colleagues [...]

scholarly journals Effects of Low-Carbohydrate versus Mediterranean Diets on Weight Loss, Glucose Metabolism, Insulin Kinetics and β-Cell Function in Morbidly Obese Individuals

Nutrients ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 1345
Author(s):  
Domenico Tricò ◽  
Diego Moriconi ◽  
Rossana Berta ◽  
Simona Baldi ◽  
Alfredo Quinones-Galvan ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Weight Loss ◽  
Cell Function ◽  
Insulin Clearance ◽  
Morbidly Obese ◽  
Β Cell ◽  
Carbohydrate Diet ◽  
Low Carbohydrate Diet ◽  
Low Carbohydrate ◽  
Β Cell Function

Low-calorie Mediterranean-style or low-carbohydrate dietary regimens are widely used nutritional strategies against obesity and associated metabolic diseases, including type 2 diabetes. The aim of this study was to compare the effectiveness of a balanced Mediterranean diet with a low-carbohydrate diet on weight loss and glucose homeostasis in morbidly obese individuals at high risk to develop diabetes. Insulin secretion, insulin clearance, and different β-cell function components were estimated by modeling plasma glucose, insulin and C-peptide profiles during 75-g oral glucose tolerance tests (OGTTs) performed at baseline and after 4 weeks of each dietary intervention. The average weight loss was 5%, being 58% greater in the low-carbohydrate-group than Mediterranean-group. Fasting plasma glucose and glucose tolerance were not affected by the diets. The two dietary regimens proved similarly effective in improving insulin resistance and fasting hyperinsulinemia, while enhancing endogenous insulin clearance and β-cell glucose sensitivity. In summary, we demonstrated that a low-carbohydrate diet is a successful short-term approach for weight loss in morbidly obese patients and a feasible alternative to the Mediterranean diet for its glucometabolic benefits, including improvements in insulin resistance, insulin clearance and β-cell function. Further studies are needed to compare the long-term efficacy and safety of the two diets.

scholarly journals Very-low-calorie diet: a quick therapeutic tool to improve β cell function in morbidly obese patients with type 2 diabetes

2012 ◽  
Vol 95 (3) ◽  
pp. 609-613 ◽  
Author(s):  
Ilaria Malandrucco ◽  
Patrizio Pasqualetti ◽  
Ilaria Giordani ◽  
Dario Manfellotto ◽  
Federica De Marco ◽  
...  
Keyword(s):  
Cell Function ◽  
Morbidly Obese ◽  
Obese Patients ◽  
Therapeutic Tool ◽  
Β Cell ◽  
Very Low Calorie Diet ◽  
Low Calorie Diet ◽  
Calorie Diet ◽  
Β Cell Function

scholarly journals Weight Loss Improves β-Cell Function in People With Severe Obesity and Impaired Fasting Glucose: A Window of Opportunity

2019 ◽  
Vol 105 (4) ◽  
pp. e1621-e1630
Author(s):  
Amy E Rothberg ◽  
William H Herman ◽  
Chunyi Wu ◽  
Heidi B IglayReger ◽  
Jeffrey F Horowitz ◽  
...  
Keyword(s):  
Weight Loss ◽  
Insulin Secretion ◽  
Insulin Sensitivity ◽  
Impaired Fasting Glucose ◽  
Severe Obesity ◽  
Cell Function ◽  
Fasting Glucose ◽  
Β Cell ◽  
Obese People ◽  
Β Cell Function

Abstract Background In people with obesity, β-cell function may adapt to insulin resistance. We describe β-cell function in people with severe obesity and normal fasting glucose (NFG), impaired fasting glucose (IFG), and type 2 diabetes (T2DM), as assessed before, 3 to 6 months after, and 2 years after medical weight loss to describe its effects on insulin sensitivity, insulin secretion, and β-cell function. Methods Fifty-eight participants with body mass index (BMI) ≥ 35 kg/m2 (14 with NFG, 24 with IFG, and 20 with T2DM) and 13 normal weight participants with NFG underwent mixed meal tolerance tests to estimate insulin sensitivity (S[I]), insulin secretion (Φ), and β-cell function assessed as model-based Φ adjusted for S(I). All 58 obese participants were restudied at 3 to 6 months and 27 were restudied at 2 years. Results At 3 to 6 months, after a 20-kg weight loss and a decrease in BMI of 6 kg/m2, S(I) improved in all obese participants, Φ decreased in obese participants with NFG and IFG and tended to decrease in obese participants with T2DM, and β-cell function improved in obese participants with NFG and tended to improve in obese participants with IFG. At 2 years, β-cell function deteriorated in participants with NFG and T2DM but remained significantly better in participants with IFG compared to baseline. Conclusions Short-term weight loss improves β-cell function in participants with NFG and IFG, but β-cell function tends to deteriorate over 2 years. In participants with IFG, weight loss improves longer-term β-cell function relative to baseline and likely relative to no intervention, suggesting that obese people with IFG are a subpopulation whose β-cell function is most likely to benefit from weight loss.

scholarly journals Sustained maternal inflammation during the early third-trimester yields intrauterine growth restriction, impaired skeletal muscle glucose metabolism, and diminished β-cell function in fetal sheep1,2

2019 ◽  
Vol 97 (12) ◽  
pp. 4822-4833 ◽  
Author(s):  
Caitlin N Cadaret ◽  
Elena M Merrick ◽  
Taylor L Barnes ◽  
Kristin A Beede ◽  
Robert J Posont ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Glucose Metabolism ◽  
Intrauterine Growth Restriction ◽  
Cell Function ◽  
Ex Vivo ◽  
White Blood Cells ◽  
Β Cell ◽  
Intrauterine Growth ◽  
Maternal Inflammation ◽  
Β Cell Function

Abstract Maternal inflammation causes fetal intrauterine growth restriction (IUGR), but its impact on fetal metabolism is not known. Thus, our objective was to determine the impact of sustained maternal inflammation in late gestation on fetal inflammation, skeletal muscle glucose metabolism, and insulin secretion. Pregnant ewes were injected every third day from the 100th to 112th day of gestation (term = 150 d) with saline (controls) or lipopolysaccharide (LPS) to induce maternal inflammation and IUGR (MI-IUGR). Fetal femoral blood vessels were catheterized on day 118 to assess β-cell function on day 123, hindlimb glucose metabolic rates on day 124, and daily blood parameters from days 120 to 125. Fetal muscle was isolated on day 125 to assess ex vivo glucose metabolism. Injection of LPS increased (P < 0.05) rectal temperatures, circulating white blood cells, and plasma tumor necrosis factor α (TNFα) concentrations in MI-IUGR ewes. Maternal leukocytes remained elevated (P < 0.05) and TNFα tended to remain elevated (P < 0.10) compared with controls almost 2 wk after the final LPS injection. Total white blood cells, monocytes, granulocytes, and TNFα were also greater (P < 0.05) in MI-IUGR fetuses than controls over this period. MI-IUGR fetuses had reduced (P < 0.05) blood O2 partial pressures and greater (P < 0.05) maternofetal O2 gradients, but blood glucose and maternofetal glucose gradients did not differ from controls. Basal and glucose-stimulated insulin secretion were reduced (P < 0.05) by 32% and 42%, respectively, in MI-IUGR fetuses. In vivo hindlimb glucose oxidation did not differ between groups under resting conditions but was 47% less (P < 0.05) in MI-IUGR fetuses than controls during hyperinsulinemia. Hindlimb glucose utilization did not differ between fetal groups. At day 125, MI-IUGR fetuses were 22% lighter (P < 0.05) than controls and tended to have greater (P < 0.10) brain/BW ratios. Ex vivo skeletal muscle glucose oxidation did not differ between groups in basal media but was less (P < 0.05) for MI-IUGR fetuses in insulin-spiked media. Glucose uptake rates and phosphorylated-to-total Akt ratios were less (P < 0.05) in muscle from MI-IUGR fetuses than controls regardless of media. We conclude that maternal inflammation leads to fetal inflammation, reduced β-cell function, and impaired skeletal muscle glucose metabolism that persists after maternal inflammation ceases. Moreover, fetal inflammation may represent a target for improving metabolic dysfunction in IUGR fetuses.

scholarly journals Maternal high-fat diet impairs glucose metabolism, β-cell function and proliferation in the second generation of offspring rats

2017 ◽  
Vol 14 (1) ◽  
Author(s):  
Yan-Hong Huang ◽  
Ting-Ting Ye ◽  
Chong-Xiao Liu ◽  
Lei Wang ◽  
Yuan-Wen Chen ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
High Fat Diet ◽  
Second Generation ◽  
Cell Function ◽  
High Fat ◽  
Β Cell ◽  
Β Cell Function
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