scholarly journals Regulation of hepatic metabolism by enteral delivery of nutrients

2006 ◽  
Vol 19 (2) ◽  
pp. 161-173 ◽  
Author(s):  
D. Dardevet ◽  
M. C. Moore ◽  
D. Remond ◽  
C. A. Everett-Grueter ◽  
A. D. Cherrington
Keyword(s):  
Amino Acids ◽  
Glucose Uptake ◽  
Nutrition Support ◽  
Whole Body ◽  
Glucose Disposal ◽  
Anatomical Location ◽  
Nutrient Metabolism ◽  
Nutrient Delivery ◽  
Hepatic Glucose ◽  
Hepatic Glucose Uptake

The liver plays a unique role in nutrient homeostasis. Its anatomical location makes it ideally suited to control the systemic supply of absorbed nutrients, and it is the primary organ that can both consume and produce substantial amounts of glucose. Moreover, it is the site of a substantial fraction (about 25 %) of the body's protein synthesis, and the liver and other organs of the splanchnic bed play an important role in sparing dietary N by storing ingested amino acids. This hepatic anabolism is under the control of hormonal and nutritional changes that occur during food intake. In particular, the route of nutrient delivery, i.e. oral (or intraportal) v. peripheral venous, appears to impact upon the disposition of the macronutrients and also to affect both hepatic and whole-body nutrient metabolism. Intraportal glucose delivery significantly enhances net hepatic glucose uptake, compared with glucose infusion via a peripheral vein. On the other hand, concomitant intraportal infusion of both glucose and gluconeogenic amino acids significantly decreases net hepatic glucose uptake, compared with infusion of the same mass of glucose by itself. Delivery of amino acids via the portal vein may enhance their hepatic uptake, however. Elevation of circulating lipids under postprandial conditions appears to impair both hepatic and whole-body glucose disposal. Thus, the liver's role in nutrient disposal and metabolism is highly responsive to the route of nutrient delivery, and this is an important consideration in planning nutrition support and optimising anabolism in vulnerable patients.

Intraportal administration of neuropeptide Y and hepatic glucose metabolism

2008 ◽  
Vol 294 (4) ◽  
pp. R1197-R1204 ◽  
Author(s):  
Makoto Nishizawa ◽  
Masakazu Shiota ◽  
Mary Courtney Moore ◽  
Stephanie M. Gustavson ◽  
Doss W. Neal ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Neuropeptide Y ◽  
Glucose Uptake ◽  
Infusion Rate ◽  
Whole Body ◽  
Glucose Disposal ◽  
Control Group ◽  
Intravenous Glucose ◽  
Hepatic Glucose ◽  
Hepatic Glucose Uptake

We examined whether intraportal delivery of neuropeptide Y (NPY) affects glucose metabolism in 42-h-fasted conscious dogs using arteriovenous difference methodology. The experimental period was divided into three subperiods (P1, P2, and P3). During all subperiods, the dogs received infusions of somatostatin, intraportal insulin (threefold basal), intraportal glucagon (basal), and peripheral intravenous glucose to increase the hepatic glucose load twofold basal. Following P1, in the NPY group ( n = 7), NPY was infused intraportally at 0.2 and 5.1 pmol·kg−1·min−1 during P2 and P3, respectively. The control group ( n = 7) received intraportal saline infusion without NPY. There were no significant changes in hepatic blood flow in NPY vs. control. The lower infusion rate of NPY (P2) did not enhance net hepatic glucose uptake. During P3, the increment in net hepatic glucose uptake (compared with P1) was 4 ± 1 and 10 ± 2 μmol·kg−1·min−1 in control and NPY, respectively ( P < 0.05). The increment in net hepatic fractional glucose extraction during P3 was 0.015 ± 0.005 and 0.039 ± 0.008 in control and NPY, respectively ( P < 0.05). Net hepatic carbon retention was enhanced in NPY vs. control (22 ± 2 vs. 14 ± 2 μmol·kg−1·min−1, P < 0.05). There were no significant differences between groups in the total glucose infusion rate. Thus, intraportal NPY stimulates net hepatic glucose uptake without significantly altering whole body glucose disposal in dogs.

scholarly journals Glucagon-mediated impairments in hepatic and peripheral tissue nutrient disposal are not aggravated by increased lipid availability

2009 ◽  
Vol 296 (5) ◽  
pp. E1172-E1178 ◽  
Author(s):  
Sheng-Song Chen ◽  
Tammy S. Santomango ◽  
Phillip E. Williams ◽  
D. Brooks Lacy ◽  
Owen P. McGuinness
Keyword(s):  
Glucose Uptake ◽  
Glucagon Secretion ◽  
Hepatic Metabolism ◽  
Whole Body ◽  
Glucose Disposal ◽  
Peripheral Tissues ◽  
Hepatic Glucose ◽  
Hepatic Glucose Uptake ◽  
Body Energy ◽  
Glucose Availability

Glucose, fat, and glucagon availability are increased in diabetes. The normal response of the liver to chronic increases in glucose availability is to adapt to become a marked consumer of glucose. Yet this fails to occur in diabetes. The aim was to determine whether increased glucagon and lipid interact to impair the adaptation to increased glucose availability. Chronically catheterized well controlled depancreatized conscious dogs ( n = 21) received 3 days of continuous parenteral nutrition (TPN) that was either high in glucose [C; 75% nonprotein calories (NPC)] or in lipid (HL; 75% NPC) in the presence or absence of a low dose (one-third basal) chronic intraportal infusion of glucagon (GN; 0.25 ng·kg−1·min−1). During the 3 days of TPN, all groups received the same insulin algorithm; the total amount of glucose infused (GIR) was varied to maintain isoglycemia (∼120 mg/dl). On day 3 of TPN, hepatic metabolism was assessed. Glucose and insulin levels were similar in all groups. GIR was decreased in HL and C + GN (∼30%) and was further decreased in HL + GN (55%). Net hepatic glucose uptake was decreased ∼15% in C + GN, and HL and was decreased ∼50% in HL + GN. Lipid alone or combined with glucagon decreased glucose uptake by peripheral tissues. Despite impairing whole body glucose utilization, HL did not limit whole body energy disposal. In contrast, glucagon suppressed whole body energy disposal irrespective of the diet composition. In summary, failure to appropriately suppress glucagon secretion adds to the dietary fat-induced impairment in both hepatic and peripheral glucose disposal. In addition, unlike increasing the percentage of calories as fat, inappropriate glucagon secretion in the absence of compensatory hyperinsulinemia limits whole body nutrient disposition.

Route-dependent effect of nutritional support on liver glucose uptake

2005 ◽  
Vol 289 (5) ◽  
pp. R1319-R1327 ◽  
Author(s):  
Sheng-Song Chen ◽  
Carlos J Torres-Sanchez ◽  
Nadeen Hosein ◽  
Yiqun Zhang ◽  
D. Brooks Lacy ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
Hepatic Metabolism ◽  
Insulin Requirement ◽  
Glucose Disposal ◽  
Nutrient Delivery ◽  
Lactate Release ◽  
Glucose Levels ◽  
Hepatic Glucose ◽  
Arterial Plasma ◽  
Hepatic Glucose Uptake

The liver is a major site of glucose disposal during chronic (5 day) total parenteral (TPN) and enteral (TEN) nutrition. Net hepatic glucose uptake (NHGU) is dependent on the route of delivery when only glucose is delivered acutely; however, the hepatic response to chronic TPN and TEN is very similar. We aimed to determine whether the route of nutrient delivery altered the acute (first 8 h) response of the liver and whether chronic enteral delivery of glucose alone could augment the adaptive response to TPN. Chronically catheterized conscious dogs received either TPN or TEN containing glucose, Intralipid, and Travasol for either 8 h or 5 days. Another group received TPN for 5 days, but ∼50% of the glucose in the nutrition was given via the enteral route (TPN+EG). Hepatic metabolism was assessed with tracer and arteriovenous difference techniques. In the presence of similar arterial plasma glucose levels (∼6 mM), NHGU and net hepatic lactate release increased approximately twofold between 8 h and 5 days in TPN and TEN. NHGU (26 ± 1 vs. 23 ± 3 μmol·kg−1·min−1) and net hepatic lactate release (44 ± 1 vs. 34 ± 6 μmol·kg−1·min−1) in TPN+EG were similar to results for TPN, despite lower insulin levels (96 ± 6 vs. 58 ± 16 pM, TPN vs. TPN+EG). TEN does not acutely enhance NHGU or disposition above that seen with TPN. However, partial delivery of enteral glucose is effective in decreasing the insulin requirement during chronic TPN.

Prevention of skeletal muscle insulin resistance by dietary cod protein in high fat-fed rats

2001 ◽  
Vol 281 (1) ◽  
pp. E62-E71 ◽  
Author(s):  
Charles Lavigne ◽  
Frédéric Tremblay ◽  
Geneviève Asselin ◽  
Hélène Jacques ◽  
André Marette
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Amino Acids ◽  
Glucose Uptake ◽  
Soy Protein ◽  
Whole Body ◽  
Glucose Disposal ◽  
High Fat ◽  
Muscle Insulin Resistance ◽  
Skeletal Muscle Insulin Resistance

In the present study, we tested the hypothesis that fish protein may represent a key constituent of fish with glucoregulatory activity. Three groups of rats were fed a high-fat diet in which the protein source was casein, fish (cod) protein, or soy protein; these groups were compared with a group of chow-fed controls. High-fat feeding led to severe whole body and skeletal muscle insulin resistance in casein- or soy protein-fed rats, as assessed by the euglycemic clamp technique coupled with measurements of 2-deoxy-d-[3H]glucose uptake rates by individual tissues. However, feeding cod protein fully prevented the development of insulin resistance in high fat-fed rats. These animals exhibited higher rates of insulin-mediated muscle glucose disposal that were comparable to those of chow-fed rats. The beneficial effects of cod protein occurred without any reductions in body weight gain, adipose tissue accretion, or expression of tumor necrosis factor-α in fat and muscle. Moreover, L6 myocytes exposed to cod protein-derived amino acids showed greater rates of insulin-stimulated glucose uptake compared with cells incubated with casein- or soy protein-derived amino acids. These data demonstrate that feeding cod protein prevents obesity-induced muscle insulin resistance in high fat-fed obese rats at least in part through a direct action of amino acids on insulin-stimulated glucose uptake in skeletal muscle cells.

Effect of intraportal glucagon-like peptide-1 on glucose metabolism in conscious dogs

2003 ◽  
Vol 284 (5) ◽  
pp. E1027-E1036 ◽  
Author(s):  
Makoto Nishizawa ◽  
Mary Courtney Moore ◽  
Masakazu Shiota ◽  
Stephanie M. Gustavson ◽  
Wanda L. Snead ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
Conscious Dogs ◽  
Glucose Disposal ◽  
Control Group ◽  
Hepatic Glucose ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Hepatic Glucose Uptake ◽  
Arteriovenous Difference ◽  
Intraportal Infusion

Arteriovenous difference and tracer ([3-3H]glucose) techniques were used in 42-h-fasted conscious dogs to identify any insulin-like effects of intraportally administered glucagon-like peptide 1-(7–36)amide (GLP-1). Each study consisted of an equilibration, a basal, and three 90-min test periods (P1, P2, and P3) during which somatostatin, intraportal insulin (3-fold basal) and glucagon (basal), and peripheral glucose were infused. Saline was infused intraportally in P1. During P2 and P3, GLP-1 was infused intraportally at 0.9 and 5.1 pmol · kg−1 · min−1in eight dogs, at 10 and 20 pmol · kg−1 · min−1in seven dogs, and at 0 pmol · kg−1 · min−1in eight dogs (control group). Net hepatic glucose uptake was significantly enhanced during GLP-1 infusion at 20 pmol · kg−1 · min−1[21.8 vs. 13.4 μmol · kg−1 · min−1(control), P < 0.05]. Glucose utilization was significantly increased during infusion at 10 and 20 pmol · kg−1 · min−1[87.3 ± 8.3 and 105.3 ± 12.8, respectively, vs. 62.2 ± 5.3 and 74.7 ± 7.4 μmol · kg−1 · min−1(control), P < 0.05]. The glucose infusion rate required to maintain hyperglycemia was increased ( P < 0.05) during infusion of GLP-1 at 5.1, 10, and 20 pmol · kg−1 · min−1(22, 36, and 32%, respectively, greater than control). Nonhepatic glucose uptake increased significantly during delivery of GLP-1 at 5.1 and 10 pmol · kg−1 · min−1(25 and 46% greater than control) and tended ( P = 0.1) to increase during GLP-1 infusion at 20 pmol · kg−1 · min−1(24% greater than control). Intraportal infusion of GLP-1 at high physiological and pharmacological rates increased glucose disposal primarily in nonhepatic tissues.

Pressor doses of angiotensin II increase insulin-mediated glucose uptake in normotensive men

1993 ◽  
Vol 265 (3) ◽  
pp. E362-E366 ◽  
Author(s):  
R. R. Townsend ◽  
D. J. DiPette
Keyword(s):  
Angiotensin Ii ◽  
Glucose Uptake ◽  
Whole Body ◽  
Glucose Disposal ◽  
Hepatic Glucose Output ◽  
Hepatic Glucose ◽  
Cast Doubt ◽  
Normotensive Subjects ◽  
Glucose Output ◽  
Biochemical Action

The effect of pressor doses of angiotensin II infused intravenously on insulin-mediated glucose uptake was determined in normotensive men. A 3-h hyperinsulinemic euglycemic clamp was employed in 14 normotensive subjects to determine insulin-mediated glucose uptake with or without an infusion of angiotensin II (approximately 15 ng.kg-1.min-1), which increased blood pressure by 20/15 mmHg (systolic/diastolic). Addition of angiotensin II increased whole body glucose uptake by 15% (9.2 +/- 0.5 vs. 10.8 +/- 0.8 mg.kg-1 x min-1; P = 0.011), and glucose oxidation (determined by indirect calorimetry) by 25% (4.0 +/- 0.3 vs. 4.9 +/- 0.4 mg.kg-1 x min-1; P < 0.05) over insulin alone. There was no significant increase in hepatic glucose output during angiotensin II infusion (2.2 +/- 0.1 vs. 2.4 +/- 0.1 mg.kg-1 x min-1; P = NS). We conclude that angiotensin II in pressor doses increases insulin-mediated glucose disposal and oxidation. The mechanism for this may involve a redirection of blood flow into skeletal muscle during angiotensin II infusion or a direct biochemical action of angiotensin II. Although performed in lean normotensive subjects, these results cast doubt on a significant role for angiotensin II in the insulin resistance associated with essential hypertension.

Fructose augments infection-impaired net hepatic glucose uptake during TPN administration

2001 ◽  
Vol 280 (5) ◽  
pp. E703-E711 ◽  
Author(s):  
Christine M. Donmoyer ◽  
Joseph Ejiofor ◽  
D. Brooks Lacy ◽  
Sheng-Song Chen ◽  
Owen P. McGuinness
Keyword(s):  
Glucose Uptake ◽  
Vena Cava ◽  
Fibrin Clot ◽  
Glycogen Storage ◽  
Glucose Disposal ◽  
Lactate Release ◽  
Hepatic Glucose Metabolism ◽  
Hepatic Glucose ◽  
Hepatic Glucose Uptake ◽  
Arteriovenous Difference

During chronic total parenteral nutrition (TPN), net hepatic glucose uptake (NHGU) and net hepatic lactate release (NHLR) are markedly reduced (↓∼45 and ∼65%, respectively) with infection. Because small quantities of fructose are known to augment hepatic glucose uptake and lactate release in normal fasted animals, the aim of this work was to determine whether acute fructose infusion with TPN could correct the impairments in NHGU and NHLR during infection. Chronically catheterized conscious dogs received TPN for 5 days via the inferior vena cava at a rate designed to match daily basal energy requirements. On the third day of TPN administration, a sterile (SHAM, n = 12) or Escherichia coli-containing (INF, n = 11) fibrin clot was implanted in the peritoneal cavity. Forty-two hours later, somatostatin was infused with intraportal replacement of insulin (12 ± 2 vs. 24 ± 2 μU/ml, SHAM vs. INF, respectively) and glucagon (24 ± 4 vs. 92 ± 5 pg/ml) to match concentrations previously observed in sham and infected animals. After a 120-min basal period, animals received either saline (Sham+S, n = 6; Inf+S, n = 6) or intraportal fructose (0.7 mg · kg−1· min−1; Sham+F, n = 6; Inf+F, n = 5) infusion for 180 min. Isoglycemia of 120 mg/dl was maintained with a variable glucose infusion. Combined tracer and arteriovenous difference techniques were used to assess hepatic glucose metabolism. Acute fructose infusion with TPN augmented NHGU by 2.9 ± 0.4 and 2.5 ± 0.3 mg · kg−1· min−1in Sham+F and Inf+F, respectively. The majority of liver glucose uptake was stored as glycogen, and NHLR did not increase substantially. Therefore, despite an infection-induced impairment in NHGU and different hormonal environments, small amounts of fructose enhanced NHGU similarly in sham and infected animals. Glycogen storage, not lactate release, was the preferential fate of the fructose-induced increase in hepatic glucose disposal in animals adapted to TPN.

Role of a negative arterial-portal venous glucose gradient in the postexercise state

1999 ◽  
Vol 277 (6) ◽  
pp. E1038-E1045 ◽  
Author(s):  
Pietro Galassetti ◽  
Yoshiharu Koyama ◽  
Robert H. Coker ◽  
Drury B. Lacy ◽  
Alan D. Cherrington ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
Vena Cava ◽  
Experimental Period ◽  
Glucose Infusion ◽  
Whole Body ◽  
Glucose Disposal ◽  
Prior Exercise ◽  
Basal Period ◽  
Hepatic Glucose ◽  
Venous Glucose

Prior exercise stimulates muscle and liver glucose uptake. A negative arterial-portal venous glucose gradient (a-pv grad) stimulates resting net hepatic glucose uptake (NHGU) but reduces muscle glucose uptake. This study investigates the effects of a negative a-pv grad during glucose administration after exercise in dogs. Experimental protocol: exercise (−180 to −30 min), transition (−30 to −20 min), basal period (−20 to 0 min), and experimental period (0 to 100 min). In the experimental period, 130 mg/dl arterial hyperglycemia was induced via vena cava (Pe, n = 6) or portal vein (Po, n = 6) glucose infusions. Insulin and glucagon were replaced at fourfold basal and basal rates. During the experimental period, the a-pv grad (mg/dl) was 3 ± 1 in Pe and −10 ± 2 in Po. Arterial insulin and glucagon were similar in the two groups. In Pe, net hepatic glucose balance (mg ⋅ kg−1⋅ min−1, negative = uptake) was 4.2 ± 0.3 (basal period) and −1.2 ± 0.3 (glucose infusion); in Po it was 4.1 ± 0.5 and −3.2 ± 0.4, respectively ( P < 0.005 vs. Pe). Total glucose infusion (mg ⋅ kg−1⋅ min−1) was 11 ± 1 in Po and 8 ± 1 in Pe ( P < 0.05). Net hindlimb and whole body nonhepatic glucose uptakes were similar. Conclusions: the portal signal independently stimulates NHGU after exercise. Conversely, prior exercise eliminates the inhibitory effect of the portal signal on glucose uptake by nonhepatic tissues. The portal signal therefore increases whole body glucose disposal after exercise by an amount equal to the increase in NHGU.

scholarly journals Hepatic and muscle glucose metabolism during total parenteral nutrition: impact of infection

1998 ◽  
Vol 275 (5) ◽  
pp. E763-E769 ◽  
Author(s):  
Owen P. McGuinness ◽  
Christine Donmoyer ◽  
Joseph Ejiofor ◽  
Suzanne McElligott ◽  
D. Brooks Lacy
Keyword(s):  
Glucose Metabolism ◽  
Parenteral Nutrition ◽  
Glucose Uptake ◽  
Total Parenteral Nutrition ◽  
Vena Cava ◽  
Glucose Disposal ◽  
Peripheral Tissues ◽  
Hepatic Glucose ◽  
Hepatic Glucose Uptake ◽  
The Impact

We examined the impact of infection on hepatic and muscle glucose metabolism in dogs adapted to chronic total parenteral nutrition (TPN). Studies were done in five conscious chronically catheterized dogs, in which sampling (artery, portal and hepatic vein, and iliac vein), infusion catheters (inferior vena cava), and Transonic flow probes (hepatic artery, portal vein, and iliac artery) were implanted. Fourteen days after surgery, dogs were placed on TPN. After 5 days of TPN, an infection was induced, and the TPN was continued. The balance of substrates across the liver and limb was assessed on the day before infection ( day 0) and 18 ( day 1) and 42 h ( day 2) after infection. On day 0, the liver was a marked net consumer of glucose (4.3 ± 0.6 mg ⋅ kg−1⋅ min−1) despite near normoglycemia (117 ± 5 mg/dl) and only mild hyperinsulinemia (16 ± 2 μU/ml). In addition, the majority (79 ± 13%) of the glucose taken up by the liver was released as lactate (34 ± 6 μmol ⋅ kg−1⋅ min−1). After infection, net hepatic glucose uptake decreased markedly on day 1(1.6 ± 0.9 mg ⋅ kg−1⋅ min−1) and remained suppressed on day 2 (2.4 ± 0.5 mg ⋅ kg−1⋅ min−1). Net hepatic lactate output also decreased on days 1 and 2 (15 ± 5 and 12 ± 3 μmol ⋅ kg−1⋅ min−1, respectively). This occurred despite increases in arterial plasma glucose on days 1 and 2 (135 ± 9 and 144 ± 9 mg/dl, respectively) and insulin levels on days 1 and 2 (57 ± 14 and 34 ± 9 μU/ml, respectively). In summary, the liver undergoes a profound adaptation to TPN, making it a major site of glucose disposal and conversion to lactate. Infection impairs hepatic glucose uptake, forcing TPN-derived glucose to be removed by peripheral tissues.

Hyperinsulinemia compensates for infection-induced impairment in net hepatic glucose uptake during TPN

2000 ◽  
Vol 279 (2) ◽  
pp. E235-E243 ◽  
Author(s):  
Christine M. Donmoyer ◽  
Sheng-Song Chen ◽  
Scott A. Hande ◽  
D. Brooks Lacy ◽  
Joseph Ejiofor ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
Critical Role ◽  
Hormone Secretion ◽  
Vena Cava ◽  
Glucose Disposal ◽  
Peripheral Tissues ◽  
Lactate Release ◽  
Time Control ◽  
Hepatic Glucose ◽  
Hepatic Glucose Uptake

In animals receiving total parenteral nutrition (TPN), infection impairs net hepatic glucose uptake (NHGU) by 40% and induces mild hyperinsulinemia. In the normal animal, the majority of the glucose taken up by the liver is diverted to lactate, but in the infected state, lactate release is curtailed. Because of the hyperinsulinemia and reduced NHGU, more glucose is utilized by peripheral tissues. Our aims were to determine the role of infection-induced hyperinsulinemia in 1) limiting the fall in NHGU and hepatic lactate release and 2) increasing the proportion of glucose disposed of by peripheral tissues. Chronically catheterized dogs received TPN for 5 days via the inferior vena cava. On day 3, a fibrin clot with a nonlethal dose of E. coli was placed into the peritoneal cavity; sham dogs received a sterile clot. On day 5, somatostatin was infused to prevent endogenous pancreatic hormone secretion, and insulin and glucagon were replaced at rates matching incoming hormone concentrations observed previously in sham or infected dogs. The TPN-derived glucose infusion was adjusted to maintain a constant arterial plasma glucose level of ∼120 mg/dl. after a basal blood sampling period, the insulin infusion rate was either maintained constant (infected time control, Hi-Ins, n = 6; sham time control, Sham, n = 6) or decreased (infected + reduced insulin, Lo-Ins; n = 6) for 180 min to levels seen in noninfected dogs (from 23 ± 2 to 12 ± 1 μU/ml). Reduction of insulin to noninfected levels decreased NHGU by 1.4 ± 0.5 mg · kg−1· min−1( P < 0.05) and nonhepatic glucose utilization by 4.8 ± 0.8 mg · kg−1· min−1( P < 0.01). The fall in NHGU was caused by a decline in HGU (Δ−0.6 ± 0.4 mg · kg−1· min−1) and a concomitant increase in hepatic glucose production (HGP, Δ0.8 ± 0.5 mg · kg−1· min−1); net hepatic lactate release was not altered. Hyperinsulinemia that accompanies infection 1) primarily diverts glucose carbon to peripheral tissues, 2) limits the fall in NHGU by enhancing HGU and suppressing HGP, and 3) does not enhance hepatic lactate release, thus favoring hepatic glucose storage. Compensatory hyperinsulinemia plays a critical role in facilitating hepatic and peripheral glucose disposal during an infection.

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