Interaction between insulin and glucose-delivery route in regulation of net hepatic glucose uptake in conscious dogs

Adkins-Marshall, Bess A.; Myers, S. R.; Hendrick, G. K.; Williams, Phillip E.; Triebwasser, K.; Floyd, B.; Cherrington, Alan D.

doi:10.2337/diabetes.39.1.87

Cited by 18 publications

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“…In a separate study, in which the hepatic glucose load was fixed at two times basal, net hepatic glucose uptake was directly dependent on the plasma insulin concentration presented to the liver; however, this effect appeared to saturate at insulin levels of 5 -6 times basal (13). Several groups have also shown that portal and oral glucose loading augment net splanchnic or hepatic glucose uptake similarly, and that both result in greater rates of glucose uptake (16.7-41.7 ixmol • k g " 1 • min~1) than are observed with peripheral glucose infusion (1,(4)(5)(6)10,(12)(13)(14)(15)(16). In the presence of hyperglycemia, the ability of portal glucose delivery to augment net hepatic glucose uptake has been observed at both basal (6) and elevated (10,13) insulin levels.…”

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confidence: 80%

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Magnitude of Negative Arterial-Portal Glucose Gradient Alters Net Hepatic Glucose Balance in Conscious Dogs

et al. 1991

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To examine the relationship between the magnitude of the negative arterial-portal glucose gradient and net hepatic glucose uptake, two groups of 42-h fasted, conscious dogs were infused with somatostatin, to suppress endogenous insulin and glucagon secretion, and the hormones were replaced intraportally to create hyperinsulinemia (3- to 4-fold basal) and basal glucagon levels. The hepatic glucose load to the liver was doubled and different negative arterial-portal glucose gradients were established by altering the ratio between portal and peripheral vein glucose infusions. In protocol 1 (n = 6) net hepatic glucose uptake was 42.2 +/- 6.7, 35.0 +/- 3.9, and 33.3 +/- 4.4 mumol.kg-1.min-1 at arterial-portal plasma glucose gradients of -4.1 +/- 0.9, -1.8 +/- 0.4, and -0.8 +/- 0.1 mM, respectively. In protocol 2 (n = 6) net hepatic glucose uptake was 26.1 +/- 2.8 and 12.2 +/- 1.7 mumol.kg-1.min-1 at arterial-portal plasma glucose gradients of -0.9 +/- 0.2 and -0.4 +/- 0.1 mM, respectively. No changes in the hepatic insulin or glucose loads were evident within a given protocol. Although net hepatic glucose uptake was lower in protocol 2 when compared with protocol 1 (26.1 +/- 2.8 vs. 33.3 +/- 4.4 mumol.kg-1.min-1) in the presence of a similar arterial-portal plasma glucose gradient (-0.9 vs. -0.8 mM) the difference could be attributed to the hepatic glucose load being lower in protocol 2 (i.e., hepatic fractional glucose extraction was not significantly different) primarily as a result of lower hepatic blood flow. In conclusion, in the presence of fixed hepatic glucose and insulin loads, the magnitude of the negative arterial-portal glucose gradient can modify net hepatic glucose uptake in vivo.

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confidence: 80%

“…and net hepatic glucose uptake in the dog was 5.5-16 ixmol • k g " 1 • min~1 (4,5,10,11). Recent studies have more clearly defined the hepatic response to changes in insulin and glucose in vivo.…”

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confidence: 96%

Magnitude of Negative Arterial-Portal Glucose Gradient Alters Net Hepatic Glucose Balance in Conscious Dogs

et al. 1991

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“…[13][14][15] Glucose uptake in the liver, however, is not insulin dependent, and increased glucose concentrations in the blood lead to increased glucose uptake by the liver. 16 Glycogen synthesis that exceeds the capacity of the liver and insulin-mediated stimulation of de novo lipogenesis both lead to an increased conversion of glucose to fatty acids. 17 As a result, increased blood glucose and free fatty acids cause a high amount of neutral fatty acid accumulation in the liver and microvesicular and macrovesicular fatty changes.…”

Section: Diet In Nafld Pathogenesismentioning

confidence: 99%

Nonalcoholic Fatty Liver Disease: A Nutritional Approach

Çolak

Tuncer²,

Şenateş³

et al. 2012

Metabolic Syndrome and Related Disorders

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Nonalcoholic fatty liver disease (NAFLD) is among the most common causes of chronic liver disease in many countries, and its prevalence is increasing. NAFLD is often considered to be a hepatic component of metabolic syndrome, and studies have established that insulin resistance plays a major role in the pathogenesis of NAFLD. Treatments for NAFLD primarily target insulin resistance. Interestingly, the most common environmental cause of insulin resistance is diet. This article examines the correlations between NAFLD and diet and provides some diet recommendations based on the most current data available.

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“…We carried out a study (42) in the conscious dog that consisted of a 30-min control period and a test period in which somatostatin was given to inhibit the endocrine pancreas, glucagon was replaced intraportally in basal amounts, and insulin was given intraportally at a rate designed to increase the insulin level fourfold (Fig. 16).…”

Section: Banting Lecture 1997mentioning

confidence: 99%

Banting Lecture 1997. Control of glucose uptake and release by the liver in vivo.

1999

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Interaction between insulin and glucose-delivery route in regulation of net hepatic glucose uptake in conscious dogs

Cited by 18 publications

References 0 publications

Magnitude of Negative Arterial-Portal Glucose Gradient Alters Net Hepatic Glucose Balance in Conscious Dogs

Magnitude of Negative Arterial-Portal Glucose Gradient Alters Net Hepatic Glucose Balance in Conscious Dogs

Nonalcoholic Fatty Liver Disease: A Nutritional Approach

Banting Lecture 1997. Control of glucose uptake and release by the liver in vivo.

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