Long-term high animal protein diet reduces body weight gain and insulin secretion in diet-induced obese rats

2012 ◽  
Vol 92 (13) ◽  
pp. 2638-2643 ◽  
Author(s):  
Haiyan Chen ◽  
Yiling Wang ◽  
Lichuan Ma ◽  
Jiajun Zhao ◽  
Yinyin Li ◽  
...  
2018 ◽  
Vol 43 (3) ◽  
pp. 265 ◽  
Author(s):  
M. A. Cholis ◽  
N. Suthama ◽  
B. Sukamto

The objective of the study was to evaluate feeding effect of microparticle protein derived from soybean meal and fish meal combined with Lactobacillus sp. at 1.2 mL on physiological condition of digestive tract and productivity of broiler. Total of 192 broiler, with initial body weight was 481.0 ± 67.2 g, given dietary treatment starting on day 21 until day 42. The experiment was assigned in a completely randomized design with 8 treatments and 4 replications. Dietary treatment were 21% intact protein (T0), 18% intact protein (T1), 21% microparticle protein (T2), 18% microparticle protein (T3), T0+Lactobacillus sp.1.2 mL (T4), T1+Lactobacillus sp.1.2 mL (T5), T2+Lactobacillus sp.1.2 mL (T6), T3+Lactobacillus sp.1.2 mL (T7). Parameters measured were total ileal lactic acid bacteria (LAB), Coliform and pH, rate of passage, daily body weight gain (DWG) and also carcass weight. Data were subjected to analysis of variance and followed by Duncan multiple range test (P<0.05). Experimental results showed that microparticle protein diet added with Lactobacillus sp. (P<0.05) increased total LAB and DWG, but decreased Coliform population, and slowed down the rate of passage. However, carcass weight was not significantly affected by treatments. Feeding microparticle protein (18%) with addition of Lactobacillus sp. (1.2 mL) can improve to be better condition of digestive tract based on higher LAB and lower Coliform populations, and increase daily body weight gain with the same carcass weight. 


2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Pauline M Smith ◽  
Charles C.T. Hindmarch ◽  
David Murphy ◽  
Alastair V. Ferguson

Nutrients ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 1045 ◽  
Author(s):  
Atsushi Masuda ◽  
Yusuke Seino ◽  
Masatoshi Murase ◽  
Shihomi Hidaka ◽  
Megumi Shibata ◽  
...  

Long-term exposure to a high starch, low-protein diet (HSTD) induces body weight gain and hyperinsulinemia concomitantly with an increase in β-cell mass (BCM) and pancreatic islets number in mice; however, the effect of short-term exposure to HSTD on BCM and islet number has not been elucidated. In the present study, we investigated changes in body weight, plasma insulin levels, BCM and islet number in mice fed HSTD for 5 weeks followed by normal chow (NC) for 2 weeks. BCM and islet number were increased in mice fed HSTD for 5 weeks compared with those in mice fed NC. On the other hand, mice fed HSTD for 5 weeks followed by NC for 2 weeks (SN) showed decreased BCM and insulin levels, compared to mice fed HSTD for 7 weeks, and no significant differences in these parameters were observed between SN and the control NC at 7 weeks. No significant difference in body weight was observed among HSTD, NC and SN fed groups. These results suggest that a high-starch diet induces an increase in BCM in a manner independent of body weight gain, and that 2 weeks of NC feeding is sufficient for the reversal of the morphological changes induced in islets by HSTD feeding.


2015 ◽  
Vol 100 (11) ◽  
pp. 1352-1361 ◽  
Author(s):  
Shanmugam M. Jeyakumar ◽  
Alex Sheril ◽  
Ayyalasomayajula Vajreswari

Endocrinology ◽  
2006 ◽  
Vol 147 (11) ◽  
pp. 5094-5101 ◽  
Author(s):  
En-Ju D. Lin ◽  
Amanda Sainsbury ◽  
Nicola J. Lee ◽  
Dana Boey ◽  
Michelle Couzens ◽  
...  

Neuropeptide Y (NPY) is a key regulator of energy homeostasis and is implicated in the development of obesity and type 2 diabetes. Whereas it is known that hypothalamic administration of exogenous NPY peptides leads to increased body weight gain, hyperphagia, and many hormonal and metabolic changes characteristic of an obesity syndrome, the Y receptor(s) mediating these effects is disputed and unclear. To investigate the role of different Y receptors in the NPY-induced obesity syndrome, we used recombinant adeno-associated viral vector to overexpress NPY in mice deficient of selective single or multiple Y receptors (including Y1, Y2, and Y4). Results from this study demonstrated that long-term hypothalamic overexpression of NPY lead to marked hyperphagia, hypogonadism, body weight gain, enhanced adipose tissue accumulation, hyperinsulinemia, and other hormonal changes characteristic of an obesity syndrome. NPY-induced hyperphagia, hypogonadism, and obesity syndrome persisted in all genotypes studied (Y1−/−, Y2−/−, Y2Y4−/−, and Y1Y2Y4−/− mice). However, triple deletion of Y1, Y2, and Y4 receptors prevented NPY-induced hyperinsulinemia. These findings suggest that Y1, Y2, and Y4 receptors under this condition are not crucially involved in NPY’s hyperphagic, hypogonadal, and obesogenic effects, but they are responsible for the central regulation of circulating insulin levels by NPY.


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