Postbinding insulin resistance around parturition in the isolated rat epitrochlearis muscle

Toyoda, Nagayasu; Deguchi, T.; Murata, K; Yamamoto, Toshihiko; Sugiyama, Yoichi

doi:10.1016/0002-9378(91)90394-7

Cited by 5 publications

(5 citation statements)

References 22 publications

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“…The 28% decrease in insulin-stimulated glucose transport (insulin-treated value minus basal value) in epitrochlearis muscles from pregnant vs. nonpregnant rats is very similar to the results of Toyoda et al (36), who found that insulin-stimulated glucose transport in isolated epitrochlearis muscles of 20-day pregnant rats was ϳ30% lower than values for nonpregnant rats. Leturque et al (27) used a euglycemic-hyperinsulinemic clamp in rats, together with injection of radiolabeled 2-deoxyglucose (2-DG), and found reduced in vivo 2-DG uptake of epitrochlearis muscles of 19-day pregnant compared with nonpregnant controls.…”

Section: Discussionsupporting

confidence: 88%

“…Earlier research demonstrated that glucose transport in insulin-stimulated epitrochlearis muscles was lower for pregnant compared with nonpregnant rats (36). The insulin dose used was known to be maximally effective for muscle from nonpregnant rats, but previous studies had not confirmed that the insulin dose was sufficient for maximally activating glucose transport by epitrochlearis muscles from insulin-resistant pregnant rats.…”

Section: Methodsmentioning

confidence: 99%

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Decreased contraction-stimulated glucose transport in isolated epitrochlearis muscles of pregnant rats

Sancho

Kim²,

Cartee³

2005

Journal of Applied Physiology

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. Decreased contraction-stimulated glucose transport in isolated epitrochlearis muscles of pregnant rats. J Appl Physiol 98: [1021][1022][1023][1024][1025][1026][1027] 2005. First published November 5, 2004; doi:10.1152/japplphysiol.00953. 2004.-Late pregnancy is characterized by insulin resistance for glucose transport in skeletal muscle. The main purpose of this study was to investigate the effect of late pregnancy on contraction-stimulated glucose transport in isolated rat skeletal muscle after in vitro electrical stimulation. Isolated epitrochlearis muscles of 19-day pregnant and aged-matched nonpregnant control rats were studied. One muscle from each rat was stimulated to contract, and the contralateral muscle served as a resting control. Tension developed during contractile activity, 3-O-methylglucose (3-MG) transport rate, and glycogen concentration were determined. Epitrochlearis muscles from other rats were used to measure insulin-stimulated 3-MG transport. There was no detectable difference between the nonpregnant and pregnant groups for contractile performance (peak tension, total tension, or fatigue). Pregnancy was not associated with significant changes in muscle glycogen concentration (resting or after contractile activity) or the contraction-stimulated decrement in glycogen concentration. For muscles from pregnant vs. nonpregnant groups, there was a 22% reduction (P Յ 0.05) in contraction-stimulated glucose transport, a 28% decrease (P Յ 0.05) in insulin-stimulated glucose transport, and unchanged basal glucose transport. In conclusion, isolated epitrochlearis muscles from pregnant vs. nonpregnant rats had a relative decrement in contraction-stimulated glucose transport that was similar to the relative decline in insulin-stimulated glucose transport. The decrement in contraction-stimulated glucose transport was not attributable to pregnancy-related changes in tension development or glycogen levels. The similar relative decline in insulin-and contraction-stimulated glucose transport raises the possibility that pregnancy impairs a distal process that is common to mechanisms whereby each stimulus activates glucose transport. insulin resistance; gestational diabetes; fatigue; glycogen LATE PREGNANCY (gestational days 18 -22 in the rat, third trimester in humans) is characterized by whole body insulin resistance (8, 27). Insulin-stimulated glucose disposal by skeletal muscle during a euglycemic-hyperinsulinemic clamp is reduced in pregnant compared with nonpregnant rats (27). Insulin resistance is also a normal characteristic of late pregnancy in humans, presumably to ensure adequate availability of maternal nutrients to the fetus during this period of rapid growth (5, 25). Toyoda et al. (36) reported decreased insulinstimulated glucose transport in isolated epitrochlearis muscles of late pregnant rats compared with nonpregnant controls, demonstrating a decrement in the intrinsic capacity for insulinstimulated glucose transport in skeletal muscle, independent of systemic factors that influence whole ...

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Section: Discussionsupporting

confidence: 88%

Section: Methodsmentioning

confidence: 99%

Decreased contraction-stimulated glucose transport in isolated epitrochlearis muscles of pregnant rats

Sancho

Kim²,

Cartee³

2005

Journal of Applied Physiology

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“…Inflammation of muscle and adipose tissue is tightly linked to insulin resistance in many metabolic scenarios (39), and these findings are the first to suggest the adaptive role of this phenomenon during early lactation. Although the dairy cow is unique in the degree of genetic selection for milk yield, postpartum insulin resistance has been documented across a broad array of wild and domestic mammals, including northern elephant seals (16), goats (14), pigs (35), and rats (10,49). We suggest that inflammatory signals underlie this conserved postpartum insulin resistance.…”

Section: R115mentioning

confidence: 86%

Anti-inflammatory salicylate treatment alters the metabolic adaptations to lactation in dairy cattle

Farney

Mamedova

Coetzee

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

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Adapting to the lactating state requires metabolic adjustments in multiple tissues, especially in the dairy cow, which must meet glucose demands that can exceed 5 kg/day in the face of negligible gastrointestinal glucose absorption. These challenges are met through the process of homeorhesis, the alteration of metabolic setpoints to adapt to a shift in physiological state. To investigate the role of inflammation-associated pathways in these homeorhetic adaptations, we treated cows with the nonsteroidal anti-inflammatory drug sodium salicylate (SS) for the first 7 days of lactation. Administration of SS decreased liver TNF-α mRNA and marginally decreased plasma TNF-α concentration, but plasma eicosanoids and liver NF-κB activity were unaltered during treatment. Despite the mild impact on these inflammatory markers, SS clearly altered metabolic function. Plasma glucose concentration was decreased by SS, but this was not explained by a shift in hepatic gluconeogenic gene expression or by altered milk lactose secretion. Insulin concentrations decreased in SS-treated cows on day 7 compared with controls, which was consistent with the decline in plasma glucose concentration. The revised quantitative insulin sensitivity check index (RQUICKI) was then used to assess whether altered insulin sensitivity may have influenced glucose utilization rate with SS. The RQUICKI estimate of insulin sensitivity was significantly elevated by SS on day 7, coincident with the decline in plasma glucose concentration. Salicylate prevented postpartum insulin resistance, likely causing excessive glucose utilization in peripheral tissues and hypoglycemia. These results represent the first evidence that inflammation-associated pathways are involved in homeorhetic adaptations to lactation.

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“…Tissue sensitivity to insulin in the liver and/or skeletal muscle may be involved, since these tissues are the major sites of insulin action in the disposal of an oral glucose load (21). In fact, skeletal muscle is insulin resistant during lactation (24), and hyperprolactinemia alters the activity of hepatic enzymes related to glucose metabolism in rats (25). Increased utilization of lipids, instead of glucose as the energy source, in the liver can be a cause of the insulin resistance in hyperprolactinemic mice (26).…”

Section: Discussionmentioning

confidence: 99%

Effect of Estrogen on Hyperprolactinemia-Induced Glucose Intolerance in SHN Mice

Matsuda

Mori

1996

Experimental Biology and Medicine

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The effects of prolactin (PRL) on circulating levels of glucose and insulin, and of estradiol on hyperprolactinemia-induced glucose intolerance of tissues were studied in pituitary-grafted SHN mice (PG mice) and sham-operated controls. Pituitary grafting (PG) decreased blood glucose levels in male mice at 1 and 3 months after the operation but did not alter those in females. PG had little effect on serum insulin levels in males, but increased those in females. In female mice at 2 months after PG, blood glucose levels were significantly higher at 1, 2, and 4 hr after glucose load when compared with those in controls. In contrast, there was no significant difference in blood glucose levels after glucose load between male PG and control mice. The rate at which blood glucose levels decreased was slower in female PG mice than in controls during the 30 min after insulin injection, whereas there was no difference in the rate after insulin injection between male PG and control mice. In ovariectomized (Ovx) mice, no significant difference was found in the blood glucose levels after a glucose load between PG and control groups at 2 months after PG. In Ovx mice treated daily with estrogen, however, a PG-dependent high level of blood glucose was observed after glucose load. These results suggest that hyperprolactinemia decreases glucose tolerance via an increase in insulin resistance in female SHN mice and that estrogen is essential to the expression of the PRL effect.

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Postbinding insulin resistance around parturition in the isolated rat epitrochlearis muscle

Cited by 5 publications

References 22 publications

Decreased contraction-stimulated glucose transport in isolated epitrochlearis muscles of pregnant rats

Decreased contraction-stimulated glucose transport in isolated epitrochlearis muscles of pregnant rats

Anti-inflammatory salicylate treatment alters the metabolic adaptations to lactation in dairy cattle

Effect of Estrogen on Hyperprolactinemia-Induced Glucose Intolerance in SHN Mice

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