251 Dietary Tryptophan Supplementation Improves Fat and Glucose Metabolism in Low Birthweight Piglets

2021 ◽  
Vol 99 (Supplement_3) ◽  
pp. 129-130
Author(s):  
Parniyan Goodarzi ◽  
Mohammad Habibi ◽  
Kennedy Roberts ◽  
Julia Sutton ◽  
Cedrick N N Shili ◽  
...  
Keyword(s):  
Phosphoenolpyruvate Carboxykinase ◽  
Low Birthweight ◽  
Glucose Transporter ◽  
Growth Parameters ◽  
Fat Metabolism ◽  
Liver Fat ◽  
Protein Abundance ◽  
Metabolic Disturbances ◽  
Meal Test ◽  
Glucose Transporter 2

Abstract Low birthweight (LBW) is associated with complications such as insulin resistance, obesity and metabolic disturbances of glucose and fat metabolism in early life. Dietary tryptophan (Trp) has been shown to reduce liver fat and suppress hyperglycemia in different species. The objective of this study was to assess the effect of dietary Trp on growth and glucose and fat metabolism in LBW pigs. Piglets (7-days old) weighing < 2 kg were considered as LBW while those weighting > 2 kg were considered as normal birthweight (NBW) and randomly allocated to 4 milk-replacer based treatments (n = 7–8): 1) NBW-0% Trp (NBW-T0), 2) LBW-0% Trp (LBW-T0), 3) LBW-0.4% Trp (LBW-T0.4), and 4) LBW-0.8% Trp (LBW-T0.8) for 3 weeks. Growth parameters and body weight were measured biweekly. At week 3, blood and tissue samples were collected in overnight-fasted pigs after a meal test. The mRNA and protein abundance of key glucose and lipid metabolism markers were determined using qPCR and western blot, respectively. Univariate GLM with Dunnett’s post-hoc test (SPSS®) was used to analyze the data. Growth parameters did not change among groups. Plasma triglycerides concentration was lower in LBW-T0.4 and LBW-T0.8 compared to LBW-T0. Blood glucose was lower in LBW-T0.8 than LBW-T0 at 60 min following the meal test. LBW-T0.8 had a lower transcript and protein abundance of liver glucose transporter-2 relative to LBW-T0. Compared to LBW-T0, LBW-T0.8 had a higher mRNA abundance of glucokinase and tended to have a lower transcript of phosphoenolpyruvate carboxykinase in liver. Relative to LBW-T0, LBW-T0.4 tended to have a lower protein abundance of sodium-glucose co-transporter 1 in jejunum. Compared to LBW-T0, LBW-T0.4 and LBW-T0.8 had a lower transcript of liver acetyl-CoA carboxylase and LBW-T0.4 had a higher transcript of liver 3-hydroxyacyl-CoA dehydrogenase. In conclusion, Trp supplementation reduced the lipogenesis and gluconeogenesis, but increased the glycolysis in LBW piglets.

scholarly journals Dietary Tryptophan Supplementation Alters Fat and Glucose Metabolism in a Low-Birthweight Piglet Model

Nutrients ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 2561
Author(s):  
Parniyan Goodarzi ◽  
Mohammad Habibi ◽  
Kennedy Roberts ◽  
Julia Sutton ◽  
Cedrick Ndhumba Shili ◽  
...  
Keyword(s):  
Feeding Behavior ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Low Birthweight ◽  
Glucose Transporter ◽  
Protein Abundance ◽  
Metabolic Complications ◽  
Glucose And Lipid Metabolism ◽  
Glucose Transporter 2 ◽  
Lower Protein ◽  
Type 3

Low birthweight (LBW) is associated with metabolic complications, such as glucose and lipid metabolism disturbances in early life. The objective of this study was to assess: (1) the effect of dietary tryptophan (Trp) on glucose and fat metabolism in an LBW piglet model, and (2) the role peripheral 5-hydroxytryptamine type 3 (5HT3) receptors in regulating the feeding behavior in LBW piglets fed with Trp-supplemented diets. Seven-day-old piglets were assigned to 4 treatments: normal birthweight-0%Trp (NBW-T0), LBW-0%Trp (LBW-T0), LBW-0.4%Trp (LBW-T0.4), and LBW-0.8%Trp (LBW-T0.8) for 3 weeks. Compared to LBW-T0, the blood glucose was decreased in LBW-T0.8 at 60 min following the meal test, and the triglycerides were lower in LBW-T0.4 and LBW-T0.8. Relative to LBW-T0, LBW-T0.8 had a lower transcript and protein abundance of hepatic glucose transporter-2, a higher mRNA abundance of glucokinase, and a lower transcript of phosphoenolpyruvate carboxykinase. LBW-T0.4 tended to have a lower protein abundance of sodium-glucose co-transporter 1 in the jejunum. In comparison with LBW-T0, LBW-T0.4 and LBW-T0.8 had a lower transcript of hepatic acetyl-CoA carboxylase, and LBW-T0.4 had a higher transcript of 3-hydroxyacyl-CoA dehydrogenase. Blocking 5-HT3 receptors with ondansetron reduced the feed intake in all groups, with a transient effect on LBW-T0, but more persistent effect on LBW-T0.8 and NBW-T0. In conclusion, Trp supplementation reduced the hepatic lipogenesis and gluconeogenesis, but increased the glycolysis in LBW piglets. Peripheral serotonin is likely involved in the regulation of feeding behavior, particularly in LBW piglets fed diets supplemented with a higher dose of Trp.

scholarly journals Functional localization of glucose transporter 2 in rat liver.

1996 ◽  
Vol 44 (11) ◽  
pp. 1231-1236 ◽  
Author(s):  
A Ogawa ◽  
K Kurita ◽  
Y Ikezawa ◽  
M Igarashi ◽  
T Kuzumaki ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Rat Liver ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Glucose Transporter ◽  
Mrna Level ◽  
Functional Difference ◽  
Isolation Technique ◽  
Glucose Transporter 2 ◽  
Normal Rat ◽  
Basolateral Plasma Membrane

Heterogeneity of zonal hepatocytes is important to elicit specific liver function. We investigated the distribution of glucose transporter 2 (GLUT-2) in normal rat liver by immunostaining and Northern blot analysis. GLUT-2 stained by immunohistochemistry was distributed predominantly in the periportal hepatocytes and gradually thinned towards the perivenous zone. Ultrastructural immunostaining of GLUT-2 showed that it was localized on microvilli of the sinusoidal plasma membrane of hepatocytes but not on the basolateral plasma membrane. Consistent with the distribution of GLUT-2 protein, the level of GLUT-2 mRNA in periportal hepatocytes was 1.9-fold higher than in perivenous hepatocytes selectively isolated by the differential isolation technique. In addition, the mRNA level of phosphoenolpyruvate carboxykinase, one of the key enzymes of gluconeogenesis, was also twofold higher in the periportal hepatocytes. These results suggest that GLUT-2 contributes to the functional difference between periportal and perivenous hepatocytes in glucose metabolism of the liver.

scholarly journals Chronic suppression of insulin by diazoxide alters the activities of key enzymes regulating hepatic gluconeogenesis in Zucker rats

2002 ◽  
pp. 871-879 ◽  
Author(s):  
R Alemzadeh ◽  
S Holshouser ◽  
P Massey ◽  
J Koontz
Keyword(s):  
Phosphoenolpyruvate Carboxykinase ◽  
Glucose Transporter ◽  
Glycogen Synthase ◽  
Zucker Rats ◽  
Hepatic Glycogen ◽  
Hepatic Gluconeogenesis ◽  
Key Enzymes ◽  
Glucose Transporter 2 ◽  
Obese Rats ◽  
Obese Zucker Rats

OBJECTIVES: Chronic attenuation of hyperinsulinemia by diazoxide (DZ), an inhibitor of glucose-mediated insulin secretion, improved insulin sensitivity and glucose tolerance and caused down-regulation of lipid metabolizing enzymes in adipose tissue and decreased the rate of weight gain in mildly hyperglycemic obese Zucker rats. Since the liver plays a central role in glucose homeostasis, we studied the effect of chronic insulin suppression on key insulin-sensitive enzymes regulating hepatic gluconeogenesis. METHODS: DZ (150 mg/kg per day) or vehicle (control) was administered to 7-week-old female obese and lean Zucker rats for a period of 4 weeks. RESULTS: DZ-treated animals showed lower fasting plasma insulin levels (P<0.001) than their controls. Plasma glucose levels were lower in DZ obese rats than in controls (P<0.001), without a significant change in DZ lean animals. DZ had no effect on glucose transporter 2 protein expression in either strain. DZ treatment resulted in lower hepatic glucokinase (P<0.001) and glucose-6-phosphatase (P<0.0001) and phosphoenolpyruvate carboxykinase (PEPCK) activities only in obese rats compared with controls (P<0.001). However, DZ-treated lean rats demonstrated higher PEPCK activity than controls (P<0.002). DZ-treated animals demonstrated enhanced hepatic glucose-6-phosphate content (P<0.01), glycogen synthase activity (P<0.0001) and glycogen content (P<0.02) compared with their controls despite increased hepatic glycogen phosphorylase a activity in these animals (P<0.02). CONCLUSIONS: Chronic suppression of hyperinsulinemia in obese Zucker rats by DZ decreased the activities of key enzymes regulating hepatic gluconeogenesis, implying that attenuation of the hyperinsulinemic state by DZ may be therapeutically beneficial.

Efficacy and cardiovascular safety of Thiazolidinediones

2020 ◽  
Vol 15 ◽  
Author(s):  
Raveendran Arkiath Veettil ◽  
Cornelius James Fernandez ◽  
Koshy Jacob
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Cardiovascular Disease ◽  
Glucose Transporter ◽  
Cell Function ◽  
Cardiovascular Safety ◽  
Cardiovascular Outcome Trials ◽  
Glucose Transporter 2 ◽  
Insulin Sensitizers

: Type 2 diabetes mellitus (T2DM) is characterized by a progressive beta cell dysfunction in the setting of peripheral insulin resistance. Insulin resistance in subjects with type 2 diabetes and metabolic syndrome is primarily caused by an ectopic fat accumulation in liver and skeletal muscle. Insulin sensitizers are particularly important in the management of T2DM. Though, thiazolidinediones (TZDs) are principally insulin sensitizers, they possess an ability to preserve pancreatic β-cell function and thereby exhibit durable glycemic control. Cardiovascular outcome trials (CVOTs) have shown that Glucagon-like-peptide 1 receptor agonists (GLP-1 RAs) and sodium glucose transporter-2 inhibitors (SGLT2i) have proven cardiovascular safety. In this era of CVOTs, drugs with proven cardiovascular (CV) safety are often preferred in patients with preexisting cardiovascular disease or at risk of cardiovascular disease. In this review, we will describe the three available drugs belonging to the TZD family, with special emphasis on their efficacy and CV safety.

SGLT-2 inhibitors: Ideal Remedy for Cardioprotection in Diabetes Mellitus.

2020 ◽  
Vol 13 ◽  
Author(s):  
Keshav Kumar ◽  
Tapan Behl ◽  
Arun Kumar ◽  
Sandeep Arora
Keyword(s):  
Diabetes Mellitus ◽  
Glucose Transporter ◽  
Clinical Trial Data ◽  
Cardiac Complications ◽  
Cardiac Inflammation ◽  
First Line Therapy ◽  
Glucose Transporter 2 ◽  
Specific Medication ◽  
Hba1c Levels

Background: A chronic metabolic disease, diabetes mellitus (DM), is associated with various comorbidity due to cardiac complications that considerably decreasing the quality of life, but there is no specific medication for this. The recent developed drugs Sodium glucose transporter 2 inhibitors (SGLT2-Is), have action on diabetes as well as on kidney. Current research and studies have shown that SGLT2-Is attenuated the risk of cardiac complication associated with morbidity and hospitalization in diabetes patients. Introduction: Sodium glucose linked transporter 2 (SGLT2) receptors are mainly situated in proximal tubule of nephron. About 90% of glucose concentration is reabsorbed by these receptors in the nephron. The advanced remedy for the management of DM is SGLT2-Is which inhibit or lower the reabsorption of glucose. Objectives: The present review explores the mechanistic principle and the clinical trial data of SGLT2-Is which further support cardioprotective effects associated with these medications. Methods: The review collaborates PUBMED, Google Scholar and Research gate databases, which were explored using keywords and their combinations such as sodium glucose co-transporter 2 inhibitors, diabetes mellitus, cardioprotective effect, empagliflozin, canagliflozin, dapagliflozin and several others, to create an eclectic manuscript. Results: SGLT2-Is showed improvement in diabetes as well as in cardiac complications. These medications decreased HbA1c levels to control hyperglycemia. The mechanism of action of these drugs showed reduction in cardiac oxidative stress, cardiac apoptosis and cardiac inflammation. Besides, SGLT-2-Is showed improvement in cardiac structure and cardiac function. Conclusion: Anti-diabetic drugs, SGLT2-Is have a protective effect against cardiac complications. This indicates that these medication could become first line therapy for cardiac patients with DM.

scholarly journals High Carbohydrate Diet Increased Glucose Transporter Protein Levels in Jejunum but Did Not Lead to Enhanced Post-Exercise Skeletal Muscle Glycogen Recovery

Nutrients ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 2140
Author(s):  
Yumiko Takahashi ◽  
Yutaka Matsunaga ◽  
Hiroki Yoshida ◽  
Terunaga Shinya ◽  
Ryo Sakaguchi ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Glucose Transporter ◽  
High Carbohydrate Diet ◽  
Oral Glucose ◽  
Carbohydrate Diet ◽  
Post Exercise ◽  
Glucose Administration ◽  
Protein Levels ◽  
High Carbohydrate ◽  
Glucose Transporter 2

We examined the effect of dietary carbohydrate intake on post-exercise glycogen recovery. Male Institute of Cancer Research (ICR) mice were fed moderate-carbohydrate chow (MCHO, 50%cal from carbohydrate) or high-carbohydrate chow (HCHO, 70%cal from carbohydrate) for 10 days. They then ran on a treadmill at 25 m/min for 60 min and administered an oral glucose solution (1.5 mg/g body weight). Compared to the MCHO group, the HCHO group showed significantly higher sodium-D-glucose co-transporter 1 protein levels in the brush border membrane fraction (p = 0.003) and the glucose transporter 2 level in the mucosa of jejunum (p = 0.004). At 30 min after the post-exercise glucose administration, the skeletal muscle and liver glycogen levels were not significantly different between the two diet groups. The blood glucose concentration from the portal vein (which is the entry site of nutrients from the gastrointestinal tract) was not significantly different between the groups at 15 min after the post-exercise glucose administration. There was no difference in the total or phosphorylated states of proteins related to glucose uptake and glycogen synthesis in skeletal muscle. Although the high-carbohydrate diet significantly increased glucose transporters in the jejunum, this adaptation stimulated neither glycogen recovery nor glucose absorption after the ingestion of post-exercise glucose.

scholarly journals Impact of SGLT2 Inhibitors on Heart Failure: From Pathophysiology to Clinical Effects

2021 ◽  
Vol 22 (11) ◽  
pp. 5863
Author(s):  
Giuseppe Palmiero ◽  
Arturo Cesaro ◽  
Erica Vetrano ◽  
Pia Clara Pafundi ◽  
Raffaele Galiero ◽  
...  
Keyword(s):  
Heart Failure ◽  
Glucose Transporter ◽  
The Elderly ◽  
Intracellular Sodium ◽  
Clinical Effects ◽  
Glucose Lowering ◽  
Beneficial Effects ◽  
Glucose Transporter 2 ◽  
Function Impairment

Heart failure (HF) affects up to over 20% of patients with type 2 diabetes (T2DM), even more in the elderly. Although, in T2DM, both hyperglycemia and the proinflammatory status induced by insulin resistance are crucial in cardiac function impairment, SGLT2i cardioprotective mechanisms against HF are several. In particular, these beneficial effects seem attributable to the significant reduction of intracellular sodium levels, well-known to exert a cardioprotective role in the prevention of oxidative stress and consequent cardiomyocyte death. From a molecular perspective, patients’ exposure to gliflozins’ treatment mimics nutrient and oxygen deprivation, with consequent autophagy stimulation. This allows to maintain the cellular homeostasis through different degradative pathways. Thus, since their introduction in the clinical practice, the hypotheses on SGLT2i mechanisms of action have changed: from simple glycosuric drugs, with consequent glucose lowering, erythropoiesis enhancing and ketogenesis stimulating, to intracellular sodium-lowering molecules. This provides their consequent cardioprotective effect, which justifies its significant reduction in CV events, especially in populations at higher risk. Finally, the updated clinical evidence of SGLT2i benefits on HF was summarized. Thus, this review aimed to analyze the cardioprotective mechanisms of sodium glucose transporter 2 inhibitors (SGLT2i) in patients with HF, as well as their clinical impact on cardiovascular events.

scholarly journals Ontology of the apelinergic system in mouse pancreas during pregnancy and relationship with β-cell mass

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Brenda Strutt ◽  
Sandra Szlapinski ◽  
Thineesha Gnaneswaran ◽  
Sarah Donegan ◽  
Jessica Hill ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Insulin Secretion ◽  
Glucose Transporter ◽  
Cell Mass ◽  
Elevated Serum ◽  
Pancreatic Β Cell ◽  
Β Cells ◽  
Β Cell ◽  
Glucose Transporter 2 ◽  
Glucose Stimulated Insulin Secretion

AbstractThe apelin receptor (Aplnr) and its ligands, Apelin and Apela, contribute to metabolic control. The insulin resistance associated with pregnancy is accommodated by an expansion of pancreatic β-cell mass (BCM) and increased insulin secretion, involving the proliferation of insulin-expressing, glucose transporter 2-low (Ins+Glut2LO) progenitor cells. We examined changes in the apelinergic system during normal mouse pregnancy and in pregnancies complicated by glucose intolerance with reduced BCM. Expression of Aplnr, Apelin and Apela was quantified in Ins+Glut2LO cells isolated from mouse pancreata and found to be significantly higher than in mature β-cells by DNA microarray and qPCR. Apelin was localized to most β-cells by immunohistochemistry although Aplnr was predominantly associated with Ins+Glut2LO cells. Aplnr-staining cells increased three- to four-fold during pregnancy being maximal at gestational days (GD) 9–12 but were significantly reduced in glucose intolerant mice. Apelin-13 increased β-cell proliferation in isolated mouse islets and INS1E cells, but not glucose-stimulated insulin secretion. Glucose intolerant pregnant mice had significantly elevated serum Apelin levels at GD 9 associated with an increased presence of placental IL-6. Placental expression of the apelinergic axis remained unaltered, however. Results show that the apelinergic system is highly expressed in pancreatic β-cell progenitors and may contribute to β-cell proliferation in pregnancy.

Sign in / Sign up

Export Citation Format

Share Document