Effect of hind limb muscle unloading on liver metabolism of rats

Stein, T. P.; Schluter, M. D.; Galante, Anthony T.; Soteropoulos, Patricia; Ramı́rez, Manuel; Bigbee, A. J.; Grindeland, R. E.; Wade, Charles E.

doi:10.1016/j.jnutbio.2004.07.003

Cited by 17 publications

(17 citation statements)

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“…As PEPCK activity in HLS mice was increased significantly suggested the increased gluconeogenesis. This observation agrees well with the study carried out by Stein et al (2005) using HLS rat on liver metabolism, where there was increased expression of pyruvate carboxylase, PEPCK and glucose 6-phosphatase of gluconeogenetic enzymes. Further, LDH activity was significantly reduced in HLS mice compared to control.…”

Section: Discussionsupporting

confidence: 92%

“…However, in our studies average body weight of simulated microgravity subjected mice (Hind limb suspension for 11 days) was found to be not different from control. In a previous study using rat model the simulated microgravity subjected animals lost body weights significantly compared to control (Stein et al 2005). This difference may be due to different rodent model system used and more days of HLS treatment (21 days).…”

Section: Discussionmentioning

confidence: 93%

“…Rodents subjected to simulated microgravity induce oxidative stress and lipid peroxidation causing damage to brain (Wise et al 2005) liver (Stein et al 2005), testis (Ding et al 2011) and muscle loss (Fitts et al 2000). Liver plays a major role in carbohydrate metabolism and the microgravity environment may have a profound effect, probably altering the regulatory enzyme activities of glycolysis and gluconeogenesis.…”

Section: Introductionmentioning

confidence: 99%

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Effect of Simulated Microgravity on the Activity of Regulatory Enzymes of Glycolysis and Gluconeogenesis in Mice Liver

Ramirez

Periyakaruppan

Sarkar

et al. 2014

Microgravity Sci. Technol.

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Gravity supports all the life activities present on earth. Microgravity environments have effect on the biological functions and physiological status of an individual. The present study was undertaken to investigate the effect of simulated microgravity on important regulatory enzymes of carbohydrate metabolism in liver using HLS mice model. Following hind limb unloading of mice for 11 days the animal's average body weights were found to be not different, while the liver weights were decreased and found to be significantly different (p < 0.005) from control mice. Further, in liver the specific activity of hexokinase enzyme was reduced (p < 0.02) and the phosphoenolpyruvate carboxykinase activity was significantly increased in simulated microgravity subjected mice compared to control (p < 0.003). Immunoblot analysis show decreased phosphofructokinase-2 activity in HLS mice compared to control. Liver lactate dehydrogenase activity significantly reduced in simulated microgravity subjected mice (p < 0.005). Thus in our study the rodents have adapted to simulated microgravity

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 93%

Section: Introductionmentioning

confidence: 99%

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Effect of Simulated Microgravity on the Activity of Regulatory Enzymes of Glycolysis and Gluconeogenesis in Mice Liver

Ramirez

Periyakaruppan

Sarkar

et al. 2014

Microgravity Sci. Technol.

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“…Thus, nitrogen disposal is inextricably linked to anaplerosis and GNG in the liver. Increased GNG has been found in many catabolic conditions, for example, in type 2 diabetes (1-3) and lung cancer (42) in humans and in muscle unloading (43) and acute uremia (44) in rats. In the latter model, GNG from alanine, glutamine, and serine was increased concomitantly with muscle protein breakdown and normalized with administration of an antiglucocorticoid, suggesting a substratedriven effect on GNG.…”

Section: Discussionmentioning

confidence: 99%

The Greater Contribution of Gluconeogenesis to Glucose Production in Obesity Is Related to Increased Whole-Body Protein Catabolism

et al. 2006

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Obesity is associated with an increase in the fractional contribution of gluconeogenesis (GNG) to glucose production. We tested if this was related to the altered protein metabolism in obesity. GNG PEP (via phosphoenol pyruvate [PEP]) was measured after a 17-h fast using the deuterated water method and 2 H nuclear magnetic resonance spectroscopy of plasma glucose. Whole-body 13 C-leucine and 3 Hglucose kinetics were measured in the postabsorptive state and during a hyperinsulinemic-euglycemic-isoaminoacidemic clamp in 19 (10 men and 9 women) lean and 16 (7 men and 9 women) obese nondiabetic subjects. Endogenous glucose production was not different between groups. Postabsorptive %GNG PEP and GNG PEP flux were higher in obese subjects, and glycogenolysis contributed less to glucose production than in lean subjects. GNG PEP flux correlated with all indexes of adiposity and with postabsorptive leucine rate of appearance (R a ) (protein catabolism). GNG PEP was negatively related to the clamp glucose rate of disposal (R d ) and to the protein anabolic response to hyperinsulinemia. In conclusion, the increased contribution of GNG to glucose production in obesity is linked to increased postabsorptive protein catabolism and insulin resistance of both glucose and protein metabolism. Due to increased protein turnover rates, greater supply of gluconeogenic amino acids to the liver may trigger their preferential use over glycogen for glucose production. Diabetes 55:675-681, 2006 T he increased fractional contribution of gluconeogenesis (GNG) to postaborptive endogenous glucose production (EGP) in type 2 diabetes is well established (1), but its role in obesity is less clear. Elevated GNG has also been reported in obesity but is associated with a smaller contribution of glycogenolysis (GLY), and hence with no increase in EGP, and therefore euglycemia (2-4). Thus, since hepatic autoregulation (5) is apparently intact in obese subjects, it is not immediately clear what mechanism is responsible for increased GNG. Such autoregulation does not appear to be intact in type 2 diabetes (2,3,6), but it remains uncertain whether it causes increased EGP as hyperglycemia increases (1)(2)(3)7,8). Insulin resistance is a hallmark of both type 2 diabetes and obesity, affecting not only glucose and lipid metabolism (9) but protein as well. We have shown that whole-body protein catabolism is increased in hyperglycemic type 2 diabetic people but improves when normoglycemia is achieved with insulin and oral antihyperglycemic agents and with hypoenergetic feeding (10,11). Recently, we reported that postabsorptive rates of endogenous leucine rate of appearance (R a ) (index of protein catabolism) are increased in obese compared with lean women (12). Further, it is well known that when the portal vein glucagon/insulin relationship favors GNG, its rate can be controlled by the supply of substrate from the periphery (9,13). Taken together, these data led us to hypothesize that elevated protein catabolism in obesity contributes to higher GNG via incr...

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“…One hypothesis is that it is an intrinsic consequence of the change in fiber type with atrophy [1]. An alternative explanation is based on altered substrate availability [19]. The coupling between muscle and liver glucose metabolism in this model could be because the change in muscle glucose metabolism is driven by substrate availability via an increase in hepatic gluconeogenesis.…”

Section: Muscle Atrophy and Energy Supplymentioning

confidence: 99%