Estimates of insulin sensitivity and β-cell function in children and adolescents with and without components of the metabolic syndrome

2017 ◽  
Vol 23 (3) ◽  
pp. 122-129
Author(s):  
Christine Frithioff-Bøjsøe ◽  
◽  
Cæcilie Trier ◽  
Cilius Esmann Fonvig, ◽  
Anne Nissen ◽  
...  
2019 ◽  
Vol 20 (7) ◽  
pp. 861-870
Author(s):  
Guo‐Hua Li ◽  
Xue‐Feng Chen ◽  
Xin‐Yi Liang ◽  
Hu Lin ◽  
Li Zhang ◽  
...  

2000 ◽  
Vol 83 (S1) ◽  
pp. S97-S102 ◽  
Author(s):  
Thomas M. S. Wolever

The metabolic syndrome represents a vicious cycle whereby insulin resistance leads to compensatory hyperinsulinaemia, which maintains normal plasma glucose but may exacerbate insulin resistance. Excess insulin secretion may eventually reduce β-cell function due to amyloid deposition, leading to raised blood glucose and further deterioration of β-cell function and insulin sensitivity via glucose toxicity. Reducing postprandial glucose and insulin responses may be a way to interrupt this process, but there is disagreement about the dietary approach to achieve this. Glucose and insulin responses are determined primarily by the amount of carbohydrate consumed and its rate of absorption. Slowly absorbed, low glycaemic-index (GI) foods are associated with increased HDL cholesterol and reduced risk of type 2 diabetes. There is some evidence that low-GI foods improve insulin sensitivity in humans, although studies using established techniques (glucose clamp or frequently sampled intravenous glucose tolerance test) have not been done. Low carbohydrate diets have been suggested to be beneficial in the treatment of the metabolic syndrome because of reduced postprandial insulin. However, they may increase fasting glucose and impair oral glucose tolerance — effects which define carbohydrate intolerance. The effects of low carbohydrate diets on insulin sensitivity depend on what is used to replace the dietary carbohydrate, and the nature of the subjects studied. Dietary carbohydrates may affect insulin action, at least in part, via alterations in plasma free fatty acids. In normal subjects a high-carbohydrate/low-GI breakfast meal reduced free fatty acids by reducing the undershoot of plasma glucose, whereas low-carbohydrate breakfasts increased postprandial free fatty acids. It is unknown if these effects occur in insulin-resistant or diabetic subjects. Thus further work needs to be done before a firm conclusion can be drawn as to the optimal amount and type of dietary carbohydrate for the treatment of the metabolic syndrome.


Obesity ◽  
2021 ◽  
Author(s):  
Anny H. Xiang ◽  
Mayra P. Martinez ◽  
Enrique Trigo ◽  
Kristina M. Utzschneider ◽  
Melanie Cree‐Green ◽  
...  

2019 ◽  
Vol 21 (1) ◽  
pp. 18-27
Author(s):  
Joon Young Kim ◽  
Hala Tfayli ◽  
Fida Bacha ◽  
SoJung Lee ◽  
Sara F. Michaliszyn ◽  
...  

Diabetes Care ◽  
2016 ◽  
Vol 40 (1) ◽  
pp. 85-93 ◽  
Author(s):  
Silva Arslanian ◽  
Laure El ghormli ◽  
Fida Bacha ◽  
Sonia Caprio ◽  
Robin Goland ◽  
...  

1998 ◽  
Vol 83 (2) ◽  
pp. 503-508
Author(s):  
Victor C. Pardini ◽  
Ivana M. N. Victória ◽  
Selma M. V. Rocha ◽  
Danielle G. Andrade ◽  
Aline M. Rocha ◽  
...  

Lipoatropic diabetes (LD) designates a group of syndromes characterized by diabetes mellitus with marked insulin resistance and either a localized or generalized absence of adipose tissue. In this study, we evaluated plasma leptin levels in subjects with congenital generalized lipoatropic diabetes (CGLD, n = 11) or acquired generalized lipoatropic diabetes (AGLD, n = 11), and assessed correlations between leptin levels and estimations of insulin secretion and insulin sensitivity using homeostasis model assessment (HOMA). Leptin levels were 0.86 ± 0.32, 1.76 ± 0.78, and 6.9 ± 4.4 ng/mL in subjects with CGLD, AGLD, and controls (n = 19), respectively (ANOVA P < 0.0001). Specific insulin levels were 154 ± 172, 177 ± 137 and 43 ± 22 pmol/L, respectively (P < 0.0001). Insulin sensitivity was significantly decreased in both groups with LD (P< 0.0001), whereas HOMA β-cell function was not significantly different when compared with controls. Leptin levels were significantly correlated with body mass index, insulin levels, and HOMA β-cell function, and inversely correlated with insulin sensitivity in control subjects but not in subjects with generalized LD. In conclusion, decreased leptin levels were observed in subjects with generalized LD, with a trend towards lower levels in the acquired than in the congenital form (P = 0.06). The temporal relationship between the decrease in leptin levels and the development of lipoatrophy should be investigated in at-risk young relatives of subjects with the acquired forms to assess the usefulness of leptin levels as a marker of lipoatrophy.


2008 ◽  
Vol 88 (3) ◽  
pp. 638-644 ◽  
Author(s):  
Sergio López ◽  
Beatriz Bermúdez ◽  
Yolanda M Pacheco ◽  
José Villar ◽  
Rocío Abia ◽  
...  

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