High Pancreatic Amylase Expression Promotes Adiposity in Obesity-Prone Carbohydrate-Sensitive Rats

2019 ◽  
Vol 149 (2) ◽  
pp. 270-279 ◽  
Author(s):  
Dalila Azzout-Marniche ◽  
Catherine Chaumontet ◽  
Julien Piedcoq ◽  
Nadezda Khodorova ◽  
Gilles Fromentin ◽  
...  

ABSTRACT Background We have reported large differences in adiposity (fat mass/body weight) gain between rats fed a low-fat, high-starch diet, leading to their classification into carbohydrate “sensitive” and “resistant” rats. In sensitive animals, fat accumulates in visceral adipose tissues, leading to the suggestion that this form of obesity could be responsible for rapid development of metabolic syndrome. Objective We investigated whether increased amylase secretion by the pancreas and accelerated starch degradation in the intestine could be responsible for this phenotype. Method Thirty-two male Wistar rats (7-wk-old) were fed a purified low-fat (10%), high-carbohydrate diet for 6 wk, in which most of the carbohydrate (64% by energy) was provided as corn starch. Meal tolerance tests of the Starch diet were performed to measure glucose and insulin responses to meal ingestion. Indirect calorimetry combined with use of 13C-labelled dietary starch was used to assess meal-induced changes in whole body and starch-derived glucose oxidation. Real-time polymerase chain reaction was used to assess mRNA expression in pancreas, liver, white and brown adipose tissues, and intestine. Amylase activity was measured in the duodenum, jejunum, and ileum contents. ANOVA and regression analyses were used for statistical comparisons. Results “Resistant” and “sensitive” rats were separated according to adiposity gain during the study (1.73% ± 0.20% compared with 4.35% ± 0.36%). Breath recovery of 13CO2 from 13C-labelled dietary starch was higher in “sensitive” rats, indicating a larger increase in whole body glucose oxidation and, conversely, a larger decrease in lipid oxidation. Amylase mRNA expression in pancreas, and amylase activity in jejunum, were also higher in sensitive rats. Conclusion Differences in digestion of starch can promote visceral fat accumulation in rats when fed a low-fat, high-starch diet. This mechanism may have important implications in human obesity.

Nutrients ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 2242
Author(s):  
José M. S. Fernández-Calleja ◽  
Lianne M. S. Bouwman ◽  
Hans J. M. Swarts ◽  
Nils Billecke ◽  
Annemarie Oosting ◽  
...  

Starches of low digestibility are associated with improved glucose metabolism. We hypothesise that a lowly digestible-starch diet (LDD) versus a highly digestible-starch diet (HDD) improves the capacity to oxidise starch, and that this is sex-dependent. Mice were fed a LDD or a HDD for 3 weeks directly after weaning. Body weight (BW), body composition (BC), and digestible energy intake (dEI) were determined weekly. At the end of the intervention period, whole-body energy expenditure (EE), respiratory exchange ratio (RER), hydrogen production, and the oxidation of an oral 13C-labelled starch bolus were measured by extended indirect calorimetry. Pancreatic amylase activity and total 13C hepatic enrichment were determined in females immediately before and 4 h after administration of the starch bolus. For both sexes, BW, BC, and basal EE and RER were not affected by the type of starch, but dEI and hydrogen production were increased by the LDD. Only in females, total carbohydrate oxidation and starch-derived glucose oxidation in response to the starch bolus were higher in LDD versus HDD mice; this was not accompanied by differences in amylase activity or hepatic partitioning of the 13C label. These results show that starch digestibility impacts glucose metabolism differently in females versus males.


1974 ◽  
Vol 82 (1) ◽  
pp. 87-95 ◽  
Author(s):  
E. F. Annison ◽  
R. Bickerstaffe ◽  
J. L. Linzell

SUMMARYThe effects of changing to a high starch: low roughage diet have been studied in two Friesian and two Jersey cows, surgically prepared for the simultaneous study of udder metabolism (arteriovenous difference x udder blood flow) and whole body turnover of milk precursors (isotope dilution).In the Friesian cows milk fat concentration was lower on the high starch diet but in the Jerseys fell only slightly in one animal. In both Friesians and in the one Jersey these changes were accompanied by an increase in total rumen VFA concentration. Rumen acetate concentration did not change but propionate doubled. Thus this confirms that the usually reported fall in ‘acetate:propionate ratio’ is due to a rise in propionate production rather than due to a fall in acetate production.There were significant falls in the blood concentrations of acetate and β-hydroxy-butyrate. The rate of extraction by the udder of acetate and β-hydroxybutyrate did not change but triglyceride extraction fell. Therefore since udder blood flow did not alter the uptake of all three fat precursors fell.The entry rate of glucose into the circulation and its contribution to total body CO2 increased. The entry rate and contribution to CO2 of acetate decreased but this was probably mainly due to a fall in endogenous acetate production by the body tissues. Plasma FFA concentration showed little change but the entry rate of palmitate fell on the high starch diet. There was also an increased proportion of unsaturated and trans fatty acids in the plasma and milk triglycerides.


2021 ◽  
Author(s):  
Liulan Zhao ◽  
Ji Liang ◽  
Lei Liao ◽  
Xiaohong Tang ◽  
Qiao Liu ◽  
...  

Abstract The intestinal barrier is primarily composed of physical, physiological and microbial barriers, and intestine microbe-immune interactions influenced by diet in fish still remain increasingly unexplored. The intestinal barriers of Largemouth bass (Micropterus salmoides) (4.1±0.2g) were explored after they were fed three different starch diets for eight weeks (low starch,7%; middle starch, 12%; high starch, 17%). The results showed that high starch diet led slight infiltration of inflammatory cells and moderate loss of mucous membrane layer in midgut. Meanwhile, high starch diet decreased the antioxidant enzymes (T-SOD) activities and genes (SOD1, SOD2, SOD3a, CAT, GPX) expression significantly (P < 0.05). The MDA content was significantly increased with increasing starch level (P < 0.05). High starch diet up-regulated the expression of pro-inflammatory genes (IL-8, IL-1β and TNFα) and apoptosis genes (bax, caspase3, caspase8 and caspase9), whereas down-regulated the expression of anti-apoptosis genes bcl-2 and tight junction proteins genes (occludin and claudin7). In addition, the high starch diet increased the relative abundance of Actinobacteria and Firmicutes, resulted in microbial dysbiosis. In conclusion, high dietary starch impaired intestinal barriers, and increased the risk of disease outbreaks.


Author(s):  
Kazuhisa Tsuchida ◽  
Akinobu Nakamura ◽  
Hideaki Miyoshi ◽  
Kelaier Yang ◽  
Yuki Yamauchi ◽  
...  

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
H. Y. Huang ◽  
R. R. Liu ◽  
G. P. Zhao ◽  
Q.H. Li ◽  
M. Q. Zheng ◽  
...  

1994 ◽  
Vol 86 (6) ◽  
pp. 677-687 ◽  
Author(s):  
J. Webber ◽  
E. Simpson ◽  
H. Parkin ◽  
I. A. MacDonald

1. The effects of acutely raising blood ketone body levels to those seen after 72 h of starvation were examined in 10 subjects after an overnight fast. Metabolic rate and respiratory exchange ratio were measured with indirect calorimetry before and during an insulin—glucose clamp. Arteriovenous differences were measured across forearm and subcutaneous abdominal adipose tissue. 2. In response to the clamp the respiratory exchange ratio rose from 0.82 to 0.83 during 3-hydroxybutyrate infusion and from 0.83 to 0.94 during control (saline) infusion (P < 0.001). 3. Forearm glucose uptake at the end of the clamp was 4.02 ± 0.95 (3-hydroxybutyrate infusion) and 7.09 ± 1.24 mmol min−1 100 ml−1 forearm (saline infusion). Whole body glucose uptake at the end of the clamp was 72.8 ± 7.9 (3-hydroxybutyrate infusion) and 51.0 ± 3.0 (saline infusion) mmol min−1 kg−1 body weight−1. 4. 3-Hydroxybutyrate infusion reduced the baseline abdominal venous—arterialized venous glycerol difference from 84 ± 28 to 25 ± 12 mmol/l and the non-esterified fatty acid difference from 0.60 ± 0.17 to 0.02 ± 0.09 mmol/l (P < 0.05 versus saline infusion). 5. Hyperketonaemia reduces adipose tissue lipolysis and decreases insulin-mediated forearm glucose uptake. Hyperketonaemia appears to prevent insulin-stimulated glucose oxidation, but does not reduce insulin-mediated glucose storage.


2017 ◽  
Vol 51 ◽  
pp. 41-45 ◽  
Author(s):  
Jo-Anne Mary Davina Murray ◽  
Sheena Brown ◽  
Peter O'Shaughnessy ◽  
Ana Monteiro ◽  
Helen Warren ◽  
...  

Endocrinology ◽  
2016 ◽  
Vol 157 (12) ◽  
pp. 4943-4960 ◽  
Author(s):  
Sandip K. Bose ◽  
Irina Hutson ◽  
Charles A. Harris

Exogenous glucocorticoid administration results in hyperglycemia, insulin resistance, hepatic dyslipidemia, and hypertension, a constellation of findings known as Cushing’s syndrome. These effects are mediated by the glucocorticoid receptor (GR). Because GR activation in liver and adipose has been implicated in metabolic syndrome (MS), we wanted to determine the role of GR in these tissues in the development of MS. Because GR knockout (KO) mice (whole-body KO) exhibit perinatal lethality due to respiratory failure, we generated tissue-specific (liver or adipose) GRKO mice using cre-lox technology. Real-time PCR analysis of liver mRNA from dexamethasone-treated wildtype (WT) and liver GRKO mice indicated that hepatic GR regulates the expression of key genes involved in gluconeogenesis and glycogen metabolism. Interestingly, we have observed that liver-specific deletion of GR resulted in a significant increase in mRNA expression of key genes involved in gluconeogenesis and glycogen metabolism in kidney tissue, indicating a compensatory mechanism to maintain glucose homeostasis. We have also observed that GR plays an important role in regulating the mRNA expression of key genes involved in lipid metabolism. Liver GRKO mice demonstrated decreased fat mass and liver glycogen content compared with WT mice administered dexamethasone for 2 weeks. Adipose-specific deletion of GR did not alter glucose tolerance or insulin sensitivity of adipose GRKO mice compared with WT mice administrated dexamethasone. This indicates that liver GR might be more important in development of MS in dexamethasone-treated mice, whereas adipose GR plays a little role in these paradigms.


Author(s):  
Paul J. Rozance ◽  
Stephanie R Wesolowski ◽  
Sonnet S. Jonker ◽  
Laura D Brown

Fetal skeletal muscle growth requires myoblast proliferation, differentiation, and fusion into myofibers in addition to protein accretion for fiber hypertrophy. Oxygen is an important regulator of this process. Therefore, we hypothesized that fetal anemic hypoxemia would inhibit skeletal muscle growth. Studies were performed in late gestation fetal sheep that were bled to anemic, and therefore hypoxemic, conditions beginning at ~125 days of gestation (term = 148 days) for 9 ± 0 days (n=19) and compared to control fetuses (n=16). A metabolic study was performed on gestational day ~134 to measure fetal protein kinetic rates. Myoblast proliferation and myofiber area were determined in biceps femoris (BF), tibialis anterior (TA), and flexor digitorum superficialis (FDS) muscles. mRNA expression of muscle regulatory factors was determined in BF. Fetal arterial hematocrit and oxygen content were 28% and 52% lower, respectively, in anemic fetuses. Fetal weight and whole-body protein synthesis, breakdown, and accretion rates were not different between groups. Hindlimb length, however, was 7% shorter in anemic fetuses. TA and FDS muscles weighed less and FDS myofiber area was smaller in anemic fetuses compared to controls. The percentage of Pax7+ myoblasts that expressed Ki67 was lower in BF and tended to be lower in FDS from anemic fetuses indicating reduced myoblast proliferation. There was less MYOD and MYF6 mRNA expression in anemic vs. control BF consistent with reduced myoblast differentiation. These results indicate that fetal anemic hypoxemia reduced muscle growth. We speculate that fetal muscle growth may be improved by strategies that increase oxygen availability.


2021 ◽  
Author(s):  
Shang-Wu Shih ◽  
Jia-Jiun Yan ◽  
Yi-Hsing Wang ◽  
Yi-Ling Tsou ◽  
Ling Chiu ◽  
...  

Estrogen-related receptors (ERRs) are known to function in mammalian kidney as key regulators of ion transport-related genes; however, a comprehensive understanding of the physiological functions of ERRs in vertebrate body fluid ionic homeostasis is still elusive. Here, we used medaka (Oryzias melastigma), a euryhaline teleost, to investigate how ERRs are involved in ion regulation. After transferring medaka from hypertonic seawater to hypotonic freshwater (FW), the mRNA expression levels of errγ2 were highly upregulated, suggesting that ERRγ2 may play a crucial role in ion uptake. In situ hybridization and immunofluorescence staining showed that errγ2 was specifically expressed in ionocytes, the cells responsible for Na+/Cl- transport. In normal FW, ERRγ2 morpholino knockdown caused reductions in the mRNA expression of Na+/Cl- cotransporter (NCC), the number of NCC ionocytes, Na+/Cl- influxes of ionocytes, and whole-body Na+/Cl- contents. In FW with low Na+ and low Cl-, the expression levels of mRNA for Na+/H+ exchanger 3 (NHE3) and NCC were both decreased in ERRγ2 morphants. Treating embryos with DY131, an agonist of ERRγ, increased the whole-body Na+/Cl- contents and ncc mRNA expression in ERRγ2 morphants. As such, medaka ERRγ2 may control Na+/Cl- uptake by regulating ncc and/or nhe3 mRNA expression and ionocyte number, and these regulatory actions may be subtly adjusted depending on internal and external ion concentrations. These findings not only provide new insights into the underpinning mechanism of actions of ERRs, but also enhance our understanding of their roles in body fluid ionic homeostasis for adaptation to changing environments during vertebrate evolution.


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