bims-glecem 2022-10-02 papers

bims-glecem

Biomed News

on Glycogen metabolism in exercise, cancer and energy metabolism

Issue of 2022–10–02
thirteen papers selected by
Dipsikha Biswas, Københavns Universitet

Hepatic overexpression of protein targeting to glycogen attenuates obesity and improves hyperglycemia in db/db mice.
Therapeutic Implications of Glycogen Synthase Kinase-3β in Alzheimer's disease: A Novel Therapeutic Target.
Molecular, Biochemical, and Clinical Characterization of Thirteen Patients with Glycogen Storage Disease 1a in Malaysia.
A novel approach to characterize phenotypic variation in GSD IV: Reconceptualizing the clinical continuum.
Sex Dimorphic Glucose Transporter-2 Regulation of Hypothalamic Astrocyte Glucose and Energy Sensor Expression and Glycogen Metabolism.
Development of breast muscle parameters, glycogen reserves, and myogenic gene expression in goslings during pre- and post-hatching periods.
Preexercise High-Fat Meal Following Carbohydrate Loading Attenuates Glycogen Utilization During Endurance Exercise in Male Recreational Runners.
A glycogen storage disease type 1a patient with type 2 diabetes.
The effect of acute manipulation of carbohydrate availability on high intensity running performance, running economy, critical speed, and substrate metabolism in trained male runners.
Exercise modifies lipid and glucose metabolism alterations induced by sleep deprivation in mice.
Resveratrol biotransformation and actions on the liver metabolism of healthy and arthritic rats.
Research Note: Divergent selection for breast muscle ultimate pH affects egg quality traits in broiler breeders.
Free-breathing 3D CEST MRI of human liver at 3.0 T.

Front Endocrinol (Lausanne). 2022 ;13 969924

Hepatic overexpression of protein targeting to glycogen attenuates obesity and improves hyperglycemia in db/db mice.

Iliana López-Soldado, Joan J Guinovart, Jordi Duran.

  Increased liver glycogen content has been shown to reduce food intake, attenuate obesity, and improve glucose tolerance in a mouse model of high-fat diet (HFD)-induced obesity. Here we studied the contribution of liver glycogen to the regulation of obesity and glucose metabolism in a model of type 2 diabetes and obesity, namely the db/db mouse. To this end, we crossed db/db mice with animals overexpressing protein targeting to glycogen (PTG) in the liver to generate db/db mice with increased liver glycogen content (db/db-PTG). Hepatic PTG overexpression reduced food intake and fat weight and attenuated obesity and hyperglycemia in db/db mice. Db/db-PTG mice showed similar energy expenditure and physical activity to db/db mice. PTG overexpression reduced liver phosphoenolpyruvate carboxykinase (PEPCK) protein levels and repressed hepatic glucose production in db/db mice. Moreover, increased liver glycogen elevated hepatic ATP content in these animals. However, lipid metabolism was not modified by PTG overexpression. In conclusion, increased liver glycogen content ameliorates the diabetic and obesity phenotype in db/db mice.

Keywords:  ATP; db/db; food intake; glucose; glycogen; liver

DOI:  https://doi.org/10.3389/fendo.2022.969924
Int J Neurosci. 2022 Sep 30. 1-27

Therapeutic Implications of Glycogen Synthase Kinase-3β in Alzheimer's disease: A Novel Therapeutic Target.

Deepa S Mandlik, Satish K Mandlik, S Arulmozhi.

  Alzheimer's disease (AD) is an extremely popular neurodegenerative condition associated with dementia, responsible for around seventy per cent of the cases. There are presently 50 million people living with dementia in the world, but this number is anticipated to increase to 152 million by 2050, posing a substantial socioeconomic encumbrance. Despite extensive research, the precise mechanisms that cause AD remain unidentified, and currently, no therapy is available. Numerous signalling paths related to AD neuropathology, including glycogen synthase kinase 3-β (GSK-3β), have been investigated as potential targets for the treatment of AD in current years.GSK-3β is a proline-directed serine/threonine kinase that is linked to a variety of biological activities, comprising glycogen metabolism to gene transcription. GSK-3β is also involved in the pathophysiology of sporadic as well as familial types of AD, which has led to the development of the GSK3 theory of AD. GSK-3β is a critical performer in the pathology of AD because dysregulation of this kinase affects all the main symbols of the disease such as amyloid formation, tau phosphorylation, neurogenesis, and synaptic and memory function. The current review highlights present-day knowledge of GSK-3β-related neurobiology, focusing on its role in AD pathogenesis signalling pathways. It also explores the possibility of targeting GSK-3β for the management of AD and offers an overview of the present research work in preclinical and clinical studies to produce GSK-3β inhibitors.

Keywords:  Alzheimer's disease; Amyloid-beta; Glycogen Synthase Kinase-3; Glycogen Synthase Kinase-3 inhibitors; Neurodegenerative diseases; Tau protein

DOI:  https://doi.org/10.1080/00207454.2022.2130297
Genet Res (Camb). 2022 ;2022 5870092

Molecular, Biochemical, and Clinical Characterization of Thirteen Patients with Glycogen Storage Disease 1a in Malaysia.

Siti Aishah Abdul Wahab, Yusnita Yakob, Mohd Khairul Nizam Mohd Khalid, Noraishah Ali, Huey Yin Leong, Lock Hock Ngu.

Background: Glycogen storage disease type 1a (GSD1a) is a rare autosomal recessive metabolic disorder characterized by hypoglycaemia, growth retardation, lactic acidosis, hepatomegaly, hyperlipidemia, and nephromegaly. GSD1a is caused by a mutation in the G6PC gene encoding glucose-6-phosphatase (G6Pase); an enzyme that catalyses the hydrolysis of glucose-6-phosphate (G6P) to phosphate and glucose.
Objective: To elaborate on the clinical findings, biochemical data, molecular genetic analysis, and short-term prognosis of 13 GSD1a patients in Malaysia.
Methods: The information about 13 clinically classified GSD1a patients was retrospectively studied. The G6PC mutation analysis was performed by PCR-DNA sequencing.
Results: Patients were presented with hepatomegaly (92%), hypoglycaemia (38%), poor weight gain (23%), and short stature (15%). Mutation analysis revealed nine heterozygous mutations; eight previously reported mutations (c.155 A > T, c.209 G > A, c.226 A > T, c.248 G > A, c.648 G > T, c.706 T > A, c.1022 T > A, c.262delG) and a novel mutation (c.325 T > C). The most common mutation found in Malaysian patients was c.648 G > T in ten patients (77%) of mostly Malay ethnicity, followed by c.248 G > A in 4 patients of Chinese ethnicity (30%). A novel missense mutation (c.325 T > C) was predicted to be disease-causing by various in silico software.
Conclusions: The establishment of G6PC molecular genetic testing will enable the detection of presymptomatic patients, assisting in genetic counselling while avoiding the invasive methods of liver biopsy.

DOI: https://doi.org/10.1155/2022/5870092
Front Genet. 2022 ;13 992406

A novel approach to characterize phenotypic variation in GSD IV: Reconceptualizing the clinical continuum.

Bridget T Kiely, Rebecca L Koch, Leticia Flores, Danielle Burner, Samantha Kaplan, Priya S Kishnani.

  Purpose: Glycogen storage disease type IV (GSD IV) has historically been divided into discrete hepatic (classic hepatic, non-progressive hepatic) and neuromuscular (perinatal-congenital neuromuscular, juvenile neuromuscular) subtypes. However, the extent to which this subtype-based classification system accurately captures the landscape of phenotypic variation among GSD IV patients has not been systematically assessed. Methods: This study synthesized clinical data from all eligible cases of GSD IV in the published literature to evaluate whether this disorder is better conceptualized as discrete subtypes or a clinical continuum. A novel phenotypic scoring approach was applied to characterize the extent of hepatic, neuromuscular, and cardiac involvement in each eligible patient. Results: 146 patients met all inclusion criteria. The majority (61%) of those with sufficient data to be scored exhibited phenotypes that were not fully consistent with any of the established subtypes. These included patients who exhibited combined hepatic-neuromuscular involvement; patients whose phenotypes were intermediate between the established hepatic or neuromuscular subtypes; and patients who presented with predominantly cardiac disease. Conclusion: The application of this novel phenotypic scoring approach showed that-in contrast to the traditional subtype-based view-GSD IV may be better conceptualized as a multidimensional clinical continuum, whereby hepatic, neuromuscular, and cardiac involvement occur to varying degrees in different patients.

Keywords:  Andersen disease; GBE1; GSD IV; glycogen branching enzyme; glycogen storage disease type IV; glycogenosis IV

DOI:  https://doi.org/10.3389/fgene.2022.992406
Neurochem Res. 2022 Sep 29.

Sex Dimorphic Glucose Transporter-2 Regulation of Hypothalamic Astrocyte Glucose and Energy Sensor Expression and Glycogen Metabolism.

Madhu Babu Pasula, Prabhat R Napit, Abdulrahman Alhamyani, Sagor C Roy, Paul W Sylvester, Khaggeswar Bheemanapally, Karen P Briski.

  The plasma membrane glucose transporter-2 (GLUT2) monitors brain cell uptake of the critical nutrient glucose, and functions within astrocytes of as-yet-unknown location to control glucose counter-regulation. Hypothalamic astrocyte-neuron metabolic coupling provides vital cues to the neural glucostatic network. Current research utilized an established hypothalamic primary astrocyte culture model along with gene knockdown tools to investigate whether GLUT2 imposes sex-specific regulation of glucose/energy sensor function and glycogen metabolism in this cell population. Data show that GLUT2 stimulates or inhibits glucokinase (GCK) expression in glucose-supplied versus -deprived male astrocytes, but does not control this protein in female. Astrocyte 5'-AMP-activated protein kinaseα1/2 (AMPK) protein is augmented by GLUT2 in each sex, but phosphoAMPKα1/2 is coincidently up- (male) or down- (female) regulated. GLUT2 effects on glycogen synthase (GS) diverges in the two sexes, but direction of this control is reversed by glucoprivation in each sex. GLUT2 increases (male) or decreases (female) glycogen phosphorylase-brain type (GPbb) protein during glucoprivation, yet simultaneously inhibits (male) or stimulates (female) GP-muscle type (GPmm) expression. Astrocyte glycogen accumulation is restrained by GLUT2 when glucose is present (male) or absent (both sexes). Outcomes disclose sex-dependent GLUT2 control of the astrocyte glycolytic pathway sensor GCK. Data show that glucose status determines GLUT2 regulation of GS (both sexes), GPbb (female), and GPmm (male), and that GLUT2 imposes opposite control of GS, GPbb, and GPmm profiles between sexes during glucoprivation. Ongoing studies aim to investigate molecular mechanisms underlying sex-dimorphic GLUT2 regulation of hypothalamic astrocyte metabolic-sensory and glycogen metabolic proteins, and to characterize effects of sex-specific astrocyte target protein responses to GLUT2 on glucose regulation.

Keywords:  AMPK; GLUT2; Glycogen; Glycogen phosphorylase; Sex differences; glucokinase

DOI:  https://doi.org/10.1007/s11064-022-03757-z
Front Physiol. 2022 ;13 990715

Development of breast muscle parameters, glycogen reserves, and myogenic gene expression in goslings during pre- and post-hatching periods.

De Xin Dang, Haizhu Zhou, Yujie Lou, Xiao Liu, Desheng Li.

  This study aimed to better understand the development patterns of breast muscle and glycogen reserves in goslings during pre- and post-hatching periods. The timepoints for sampling were embryonic days 23 and 27 of hatching and days 1, 4, and 7 post hatching. We found that the body weight of goslings increased with age. The small intestine developed with age and remained reasonably constant on day 4 post hatching. The breast muscle development decreased with age and stayed relatively stable on day 1 post hatching. The diameter of myofiber increased prior to hatching and then decreased while hatching. The development patterns of breast muscle glycogen reserves were similar to the diameter of myofiber. In contrast, the contents of liver glycogen began to decrease before hatching and then increased rapidly after hatching. Moreover, the expression of Myf-5 increased with age. The expression of MSTN was maintained at high levels prior to hatching, dropped immediately after hatching, and then gradually increased with age. Additionally, we also observed that the glycogen content in the breast muscle was positively correlated with the diameter of the myofiber. The liver glycogen content was positively correlated to the relative weight of the breast muscle, the diameter of the myofiber, and the breast muscle glycogen content. The development pattern of the myofiber was synchronized with the change in the MSTN/Myf-5 ratio. This study provided a profile to understand the development patterns of breast muscle, glycogen reserves, and myogenic gene expression in goslings, which was beneficial to understanding the characteristics of energy reserves during the early life of goslings.

Keywords:  breast; early-life development; glycogen; gosling; myogenic gene

DOI:  https://doi.org/10.3389/fphys.2022.990715
J Strength Cond Res. 2022 Sep 22.

Preexercise High-Fat Meal Following Carbohydrate Loading Attenuates Glycogen Utilization During Endurance Exercise in Male Recreational Runners.

Kaito Iwayama, Yoko Tanabe, Katsuhiko Yajima, Fumiya Tanji, Takahiro Onishi, Hideyuki Takahashi.

ABSTRACT: Iwayama, K, Tanabe, Y, Yajima, K, Tanji, F, Onishi, T, and Takahashi, H. Preexercise high-fat meal following carbohydrate loading attenuates glycogen utilization during endurance exercise in male recreational runners. J Strength Cond Res XX(X): 000-000, 2022-This study aimed to investigate whether one preexercise high-fat meal can increase glycogen conservation during endurance exercise, as compared with one preexercise high-carbohydrate meal. Ten young male recreational runners (22.0 ± 0.6 years; 171.3 ± 0.9 cm; 58.3 ± 1.9 kg; maximal oxygen uptake [V̇o2max], 62.0 ± 1.6 ml·kg-1·min-1) completed 2 exercise trials after high-carbohydrate loading: eating a high-carbohydrate (CHO; 7% protein, 13% fat, 80% carbohydrate) meal or eating a high-fat (FAT; 7% protein, 42% fat, 52% carbohydrate) meal 3.5 hours before exercise. The order of the 2 trials was randomized, and the interval between trials was at least 1 week. The experimental exercise consisted of running on a treadmill for 60 minutes at 95% of each subject's lactate threshold. Muscle and liver glycogen content were assessed using noninvasive carbon magnetic resonance spectroscopy before the experimental meal as well as before and after exercise; respiratory gases were measured continuously during exercise. The respiratory exchange ratio during exercise was statistically lower in the FAT trial than in the CHO trial (p < 0.01). In addition, muscle (p < 0.05) and liver (p < 0.05) glycogen utilization during exercise was less in the FAT trial than in the CHO trial. Therefore, one high-fat meal following carbohydrate loading reduced muscle and liver glycogen use during the 60-minute exercise. These results suggest that this dietary approach may be applied as a strategy to optimize energy utilization during endurance exercise.

DOI: https://doi.org/10.1519/JSC.0000000000004311
BMC Med Genomics. 2022 Sep 27. 15(1): 205

A glycogen storage disease type 1a patient with type 2 diabetes.

Yi Sun, Wenhui Qiang, Runze Wu, Tong Yin, Jie Yuan, Jin Yuan, Yunjuan Gu.

   BACKGROUND: Glycogen storage disease type 1a (GSD1a) is an inborn genetic disease caused by glucose-6-phosphatase-α (G6Pase-α) deficiency and is often observed to lead to endogenous glucose production disorders manifesting as hypoglycemia, hyperuricemia, hyperlipidemia, lactic acidemia, hepatomegaly, and nephromegaly. The development of GSD1a with diabetes is relatively rare, and the underlying pathogenesis remains unclear.
CASE PRESENTATION: Here we describe a case of a 25-year-old Chinese female patient with GSD1a, who developed uncontrolled type 2 diabetes mellitus (T2DM) as a young adult. The patient was diagnosed with GSD1a disease at the age of 10 and was subsequently treated with an uncooked cornstarch diet. Recently, the patient was treated in our hospital for vomiting and electrolyte imbalance and was subsequently diagnosed with T2DM. Owing to the impaired secretory function of the patient's pancreatic islets, liver dysfunction, hypothyroidism, severe hyperlipidemia, and huge hepatic adenoma, we adopted diet control, insulin therapy, and hepatic adenoma resection to alleviate this situation. The WES discovered compound heterozygous mutations at the exon 5 of G6PC gene at 17th chromosome in the patient, c.648G>T (p.L216 L, NM_000151.4, rs80356484) in her father and c.674T>C (p.L225 P, NM_000151.4, rs1555560128) in her mother. c.648G>T is a well-known splice-site mutation, which causes CTG changing to CTT at protein 216 and creates a new splicing site 91 bp downstream of the authentic splice site, though both codons encode leucine. c.674T>C is a known missense mutation that causes TGC to become CGC at protein 225, thereby changing from coding for leucine to coding for proline.
CONCLUSION: We report a rare case of GSD1a with T2DM. On the basis of the pathogenesis of GSD1a, we recommend attentiveness to possible development of fasting hypoglycemia caused by GSD and postprandial hyperglycemia from diabetes. As the disease is better identified and treated, and as patients with GSD live longer, this challenge may appear more frequently. Therefore, it is necessary to have a deeper and more comprehensive understanding of the pathophysiology of the disease and explore suitable treatment options.

Keywords:  G6PC gene; GSD1a; T2DM

DOI:  https://doi.org/10.1186/s12920-022-01344-3
Eur J Sport Sci. 2022 Sep 28. 1-23

The effect of acute manipulation of carbohydrate availability on high intensity running performance, running economy, critical speed, and substrate metabolism in trained male runners.

Andrius Ramonas, Paul B Laursen, Micalla Williden, Andrew E Kilding.

  Completing selected training sessions with reduced glycogen availability is associated with greater signalling and improved muscle oxidative capacity, although it may impact the overall quality of the session. We examined the effects of low carbohydrate availability on high intensity exercise performance, running economy, critical speed, and substrate metabolism. On two occasions, nine male runners (V̇O2peak 60.3 ± 3.3 mL.kg-1.min-1) completed a glycogen depletion protocol involving 90-min at 75%vV̇O2peak followed by 10 × 1-min at 110% vV̇O2peak. This was followed either by high (HIGH) or low (LOW) carbohydrate intake (>6 g.kg-1.day-1 and <50 g.day-1, respectively) until completion of a performance protocol on day 2 consisting of a series of time-trials (TT) (50m to 3000m) and physiological assessments. There were no differences between LOW and HIGH for any TT distance (mean TT performance times for LOW and HIGH were: 3000m TT 651.7 ± 52.8s and 646.4 ± 52.5s, 1500 m TT 304.0 ± 20.2s and 304.2 ± 22.1s, 400 m TT 67.64 ± 4.2s and 67.3 ± 3.8s, 50 m TT 7.27 ± 0.44s and 7.25 ± 0.45s, respectively, P > 0.05), though some athletes performed better in LOW (n = 5). While fat oxidation in LOW was significantly greater than HIGH (Δ0.32 ± 0.14 g.min-1; P < 0.001 at 14 km.h-1 and Δ0.34 ± 0.12 g.min-1 at 16 km.h-1; P < 0.01), running economy did not differ between trials (P > 0.05). Acute manipulation of carbohydrate availability showed immediate effects on substrate metabolism evidenced by greater fat oxidation without changes in RE. Acute low carbohydrate availability did not affect high intensity running performance across a range of distances.

Keywords:  low glycogen; periodised nutrition; substrate metabolism

DOI:  https://doi.org/10.1080/17461391.2022.2130097
Sleep Sci. 2022 Jul-Sep;15(3):15(3): 347-350

Exercise modifies lipid and glucose metabolism alterations induced by sleep deprivation in mice.

Bruna Rafaele Diogenes da Silva, Paulo Iury Gomes Nunes, Flavia Almeida Santos, Pedro Felipe Carvalhedo de Bruin, Veralice Meireles Sales de Bruin.

  Insufficient sleep compromises lipid/glucose homeostasis. In opposition, exercise increases energy expenditure and has positive effects on glucose and fatty acid metabolism. Presently, it is hypothesized that exercise ameliorates metabolic dysfunction associated with sleep deprivation (SD). The effects of exercise (EX), SD and EX before SD. (EX+SD) on lipid and glucose metabolism were evaluated. Swiss mice were assigned to 4 groups (N=12, each) control, exercise (EX, 8 weeks, 1-hour of treadmill/9cm/s, 5x/week, from noon to 1:00 p.m.), SD (SD-72h, multiple platforms method), and exercise before SD (EX+SD). Exercise increased blood glucose, lactate and triglycerides (p<0.05). Both, SD and EX+SD reduced blood triglycerides (p<0.05). EX increased VLDL and reduced LDL; conversely, SD and EX+SD reduced VLDL and increased LDL. Hepatic triglycerides were markedly reduced by SD (p<0.05) and this was prevented by previous exercise (EX+SD). In summary, exercise improved essential cholesterol fractions and exercise before SD increased hepatic cholesterol and prevented hepatic triglycerides depletion.

Keywords:  Cholesterol; Exercise; Glycogen; Lipids; Liver; Sleep Deprivation

DOI:  https://doi.org/10.5935/1984-0063.20220061
Life Sci. 2022 Sep 23. pii: S0024-3205(22)00691-9. [Epub ahead of print] 120991

Resveratrol biotransformation and actions on the liver metabolism of healthy and arthritic rats.

Mellina S Simões, Ana Paula Ames-Sibin, Emanuele P Lima, Vanesa O Pateis, Ciomar A Bersani-Amado, Paulo C F Mathias, Rosane M Peralta, Anacharis B Sá-Nakanishi, Lívia Bracht, Adelar Bracht, Jurandir F Comar.

   AIMS: To investigate the effects of resveratrol on glycogen catabolism and gluconeogenesis in perfused livers of healthy and arthritic rats. The actions of resveratrol-3-O-glucuronide (R3G) and the biotransformation of resveratrol into R3G was further evaluated in the livers.
MAIN METHODS: arthritis was induced with Freund's adjuvant. Resveratrol at concentrations of 10, 25, 50, 100 and 200 μM and 200 μM R3G were introduced in perfused livers. Resveratrol and metabolites were measured in the outflowing perfusate. Respiration of isolated mitochondria and activity of gluconeogenic enzymes were also evaluated in the livers.
KEY FINDINGS: resveratrol inhibited glycogen catabolism when infused at concentrations above 50 μM and gluconeogenesis even at 10 μM in both healthy and arthritic rat livers, but more sensitive in these latter. Resveratrol above 100 μM inhibited ADP-stimulated respiration and the activities of NADH- and succinate-oxidases in mitochondria, which were partially responsible for gluconeogenesis inhibition. Pyruvate carboxylase activity was inhibited by 25 μM resveratrol and should inhibit gluconeogenesis already at low concentrations. Resveratrol was significantly metabolized to R3G in healthy rat livers, however, R3G formation was lower in arthritic rat livers. The latter must be in part a consequence of a lower glucose disposal for glucuronidation. When compared to resveratrol, R3G inhibited gluconeogenesis in a lower extension and glycogen catabolism in a higher extension.
SIGNIFICANCE: the effects of resveratrol and R3G tended to be transitory and existed only when the resveratrol is present in the organ, however, they should be considered because significant serum concentrations of both are found after oral ingestion of resveratrol.

Keywords:  Gluconeogenesis; Liver metabolism; Pyruvate carboxylase; Resveratrol; Resveratrol glucuronide; Rheumatoid arthritis

DOI:  https://doi.org/10.1016/j.lfs.2022.120991
Poult Sci. 2022 Aug 27. pii: S0032-5791(22)00431-X. [Epub ahead of print]101(11): 102142

Research Note: Divergent selection for breast muscle ultimate pH affects egg quality traits in broiler breeders.

Kadir Erensoy, Emilie Raynaud, Angélique Petit, Yannick Baumard, Sonia Métayer-Coustard, Elisabeth Le Bihan-Duval.

  Two divergently selected broiler lines were created by selection for low (pHu-) or high (pHu+) Pectoralis major ultimate pH (pHu) in order to better understand the molecular mechanisms underlying meat quality traits in broilers and are also unique genetic resources reflecting low and high glycogen levels in chicken muscle. The present study aimed to reveal the correlated phenotypical changes of egg quality traits in broiler breeders from the 2 divergent lines at the 14th generation. Birds were reared on littered floor system until 18 wk of age and in individual cages up to 42 wk. Individual egg production was recorded daily from age at first egg to 42 wk. External (egg weight: EW and shape index: SI), internal (albumen height: AH, Haugh unit: HU, yolk index: YI, and yolk color: YC), and shell (shell percentage: ESP, thickness: EST and strength: ESS) characteristics of eggs in pHu- and pHu+ lines were measured in all eggs for 4 consecutive days at 26, 27, 28, 30, 31, 32, 41, and 42 wk of age. The pHu- line had significantly higher egg percentage than pHu+ (55.9 and 49.1%, respectively). The EW in pHu- line (57.2 g) was significantly lower than in pHu+ (59.0 g) and increased with age in both lines. The mean ESP, EST and ESS were lower in the pHu+ eggs compared to the pHu- line. ESP and EST decreased mainly from 26 to 27 wk of age and they had a stable trend with advancing age in the remaining weeks. AH and YI were lower in pHu- line eggs than in pHu+. YC was more intense and HU higher in pHu+ eggs than pHu- in pre-peak and peak laying period. In conclusion, these results showed that a divergent selection for muscle energy metabolism has led to correlated responses on internal and external egg quality traits and suggest that the production of good-quality eggs may be impaired in broiler breeders with low energy reserves.

Keywords:  broiler; egg quality; meat quality; metabolism; muscle glycogen

DOI:  https://doi.org/10.1016/j.psj.2022.102142
Magn Reson Med. 2022 Sep 25.

Free-breathing 3D CEST MRI of human liver at 3.0 T.

Pei Han, Karandeep Cheema, Tianle Cao, Hsu-Lei Lee, Fei Han, Nan Wang, Hui Han, Yibin Xie, Anthony G Christodoulou, Debiao Li.

   PURPOSE: To develop a novel 3D abdominal CEST MRI technique at 3 T using MR multitasking, which enables entire-liver coverage with free-breathing acquisition.
METHODS: k-Space data were continuously acquired with repetitive steady-state CEST (ss-CEST) modules. The stack-of-stars acquisition pattern was used for k-space sampling. MR multitasking was used to reconstruct motion-resolved 3D CEST images of 53 frequency offsets with entire-liver coverage and 2.0 × 2.0 × 6.0 mm3 spatial resolution. The total scan time was 9 min. The sensitivity of amide proton transfer (APT)-CEST (magnetization transfer asymmetry [MTRasym ] at 3.5 ppm) and glycogen CEST (glycoCEST) (mean MTRasym around 1.0 ppm) signals generated with the proposed method were tested with fasting experiments.
RESULTS: Both APT-CEST and glycoCEST signals showed high sensitivity between post-fasting and post-meal acquisitions. APT-CEST and glycoCEST MTRasym signals from post-mean scans were significantly increased (APT-CEST: -0.019 ± 0.017 in post-fasting scans, 0.014 ± 0.021 in post-meal scans, p < 0.01; glycoCEST: 0.003 ± 0.009 in post-fasting scans, 0.027 ± 0.021 in post-meal scans, p < 0.01).
CONCLUSION: The proposed 3D abdominal steady-state CEST method using MR multitasking can generate CEST images of the entire liver during free breathing.

Keywords:  APT; MR multitasking; chemical exchange saturation transfer; glycogen; liver; steady-state CEST

DOI:  https://doi.org/10.1002/mrm.29470