scholarly journals A high-fat, high-saturated fat diet decreases insulin sensitivity without changing intra-abdominal fat in weight-stable overweight and obese adults

2015 ◽  
Vol 7 (S1) ◽  
Author(s):  
Anize Delfino von Frankenberg ◽  
Anna Marina ◽  
Xiaoling Song ◽  
Holly S Callahan ◽  
Mario Kratz ◽  
...  
2015 ◽  
Vol 56 (1) ◽  
pp. 431-443 ◽  
Author(s):  
Anize D. von Frankenberg ◽  
Anna Marina ◽  
Xiaoling Song ◽  
Holly S. Callahan ◽  
Mario Kratz ◽  
...  

2017 ◽  
Vol 232 (1) ◽  
pp. 49-57 ◽  
Author(s):  
Charlene Diepenbroek ◽  
Leslie Eggels ◽  
Mariëtte T Ackermans ◽  
Eric Fliers ◽  
Andries Kalsbeek ◽  
...  

We showed previously that rats on a free-choice high-fat, high-sugar (fcHFHS) diet become rapidly obese and develop glucose intolerance within a week. Interestingly, neither rats on a free-choice high-fat diet (fcHF), although equally obese and hyperphagic, nor rats on a free-choice high-sugar (fcHS) diet consuming more sugar water, develop glucose intolerance. Here, we investigate whether changes in insulin sensitivity contribute to the observed glucose intolerance and whether this is related to consumption of saturated fat and/or sugar water. Rats received either a fcHFHS, fcHF, fcHS or chow diet for one week. We performed a hyperinsulinemic–euglycemic clamp with stable isotope dilution to measure endogenous glucose production (EGP; hepatic insulin sensitivity) and glucose disappearance (Rd; peripheral insulin sensitivity). Rats on all free-choice diets were hyperphagic, but only fcHFHS-fed rats showed significantly increased adiposity. EGP suppression by hyperinsulinemia in fcHF-fed and fcHFHS-fed rats was significantly decreased compared with chow-fed rats. One week fcHFHS diet also significantly decreased Rd. Neither EGP suppression nor Rd was affected in fcHS-fed rats. Our results imply that, short-term fat feeding impaired hepatic insulin sensitivity, whereas short-term consumption of both saturated fat and sugar water impaired hepatic and peripheral insulin sensitivity. The latter likely contributed to glucose intolerance observed previously. In contrast, overconsumption of only sugar water affected insulin sensitivity slightly, but not significantly, in spite of similar adiposity as fcHF-fed rats and higher sugar intake compared with fcHFHS-fed rats. These data imply that the palatable component consumed plays a role in the development of site-specific insulin sensitivity.


Diabetologia ◽  
2002 ◽  
Vol 45 (3) ◽  
pp. 369-377 ◽  
Author(s):  
L. K. M. Summers ◽  
B. A. Fielding ◽  
H. A. Bradshaw ◽  
V. Ilic ◽  
C. Beysen ◽  
...  

2014 ◽  
Vol 144 (11) ◽  
pp. 1753-1759 ◽  
Author(s):  
Sally Chiu ◽  
Paul T. Williams ◽  
Taylor Dawson ◽  
Richard N. Bergman ◽  
Darko Stefanovski ◽  
...  

2019 ◽  
Vol 31 (3) ◽  
pp. 212-218

Both insulin and leptin are major contributors for the body energy balance. Obesity is a state of energy imbalance and is also associated with changes in both insulin sensitivity and leptin sensitivity. The aim of this study was to find out the relationship between insulin sensitivity and body fat composition, and leptin sensitivity in non-obese and obese adults. A total of 86 adults participated: 42 non-obese and 44 over-weight/obese. Body fat (BF) percent was determined by skinfold method. Fasting plasma glucose was analyzed by glucose oxidase-phenol and 4 aminophenazone (GOD-PAP) method using spectro-photometer, fasting serum insulin and leptin concentrations by direct sandwich ELISA method and resting energy expenditure (REE) by indirect calorimetry. Leptin sensitivity index and insulin sensitivity were expressed as REE : Leptin ratio and homeostatic model assessment-insulin resistance (HOMA-IR), respectively. It was found that median value of HOMA-IR was significantly higher [2.93 vs 1.72, p<0.01] and leptin sensitivity was significantly lower [116.76 vs 265.66, p<0.001] in the overweight/obese adults than the non-obese adults, indicating that insulin sensitivity and leptin sensitivity were markedly reduced in overweight/obese adults in compare to non-obese adults. There was a moderate degree of positive relationship between HOMA-IR and BF only in the overweight/obese (ρ=0.509, n=44, p<0.001) and all adults (ρ=0.39, n=86, p<0.001). Similarly, a weak negative relationship between leptin sensitivity index and HOMA-IR was found in the overweight/obese (ρ=-0.328, n=44, p<0.05) and all adults (ρ=-0.35, n=86, p<0.01). It can be concluded that the insulin sensitivity was adiposity dependent, but, it did not depend on leptin sensitivity.


2021 ◽  
Vol 22 (10) ◽  
pp. 5390
Author(s):  
Qianhui Zeng ◽  
Nannan Wang ◽  
Yaru Zhang ◽  
Yuxuan Yang ◽  
Shuangshuang Li ◽  
...  

Obesity-induced adipose tissue dysfunction and disorders of glycolipid metabolism have become a worldwide research priority. Zfp217 plays a crucial role in adipogenesis of 3T3-L1 preadipocytes, but about its functions in animal models are not yet clear. To explore the role of Zfp217 in high-fat diet (HFD)-induced obese mice, global Zfp217 heterozygous knockout (Zfp217+/−) mice were constructed. Zfp217+/− mice and Zfp217+/+ mice fed a normal chow diet (NC) did not differ significantly in weight gain, percent body fat mass, glucose tolerance, or insulin sensitivity. When challenged with HFD, Zfp217+/− mice had less weight gain than Zfp217+/+ mice. Histological observations revealed that Zfp217+/− mice fed a high-fat diet had much smaller white adipocytes in inguinal white adipose tissue (iWAT). Zfp217+/− mice had improved metabolic profiles, including improved glucose tolerance, enhanced insulin sensitivity, and increased energy expenditure compared to the Zfp217+/+ mice under HFD. We found that adipogenesis-related genes were increased and metabolic thermogenesis-related genes were decreased in the iWAT of HFD-fed Zfp217+/+ mice compared to Zfp217+/− mice. In addition, adipogenesis was markedly reduced in mouse embryonic fibroblasts (MEFs) from Zfp217-deleted mice. Together, these data indicate that Zfp217 is a regulator of energy metabolism and it is likely to provide novel insight into treatment for obesity.


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