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Comparison of Insulin Action on Glucose versus
Potassium Uptake in Humans
Trang Q. Nguyen,*
†
Naim M. Maalouf,*
†
Khashayar Sakhaee,*
†
and Orson W. Moe*
†‡
Summary
Background and objectives Insulin has several physiologic actions that include stimulation of cellular glu-
cose and potassium uptake. The ability of insulin to induce glucose uptake by cells is impaired in type 2
diabetes mellitus, but whether potassium uptake is similarly impaired is not known. This study examines
whether the cellular uptake of these molecules is regulated in concert or independently.
Design, setting, participants, & measurements Thirty-two nondiabetic and 13 type 2 diabetic subjects with
normal GFR were given a similar, constant metabolic diet for 8 days. On day 9, they were subjected to a
hyperinsulinemic euglycemic clamp for 2 hours. Serum and urinary chemistry were obtained before and
during the clamp. Glucose disposal rate was calculated from glucose infusion rate during hyperinsulinemic
euglycemia. Intracellular potassium and phosphate uptake were calculated by the reduction of extracellular
potassium or phosphate content corrected for urinary excretion.
Results Although glucose disposal rate tended to be lower in type 2 diabetics, cellular potassium uptake
was similar between diabetics and nondiabetics. Additionally, although glucose disposal rate was lower
with increasing body mass index (R
2
⫽0.362), cellular potassium (R
2
⫽0.052), and phosphate (R
2
⫽0.002),
uptake rates did not correlate with body mass index. There was also no correlation between glucose dis-
posal rate and potassium (R
2
⫽0.016) or phosphate uptake (R
2
⫽0.053).
Conclusions Insulin-stimulated intracellular uptake of glucose and potassium are independent of each other.
In type 2 diabetes, potassium uptake is preserved despite impaired glucose disposal.
Clin J Am Soc Nephrol 6: 1533–1539, 2011. doi: 10.2215/CJN.00750111
Introduction
Insulin has a multitude of actions on a wide range of
cellular processes. In terms of caloric and glucose
metabolism, insulin suppresses glycogenolysis, glu-
coneogenesis, lipolysis and fatty acid release, and pro-
tein catabolism and is the principal hormone that
stimulates glucose uptake into mainly skeletal muscle
and to a certain extent adipocytes (1–6). In subjects
with the metabolic syndrome or type 2 diabetes, in-
sulin-stimulated glucose uptake is impaired (7), a
condition frequently termed “insulin resistance” in
common clinical parlance, although not all insulin
actions are necessarily impaired.
Serum potassium concentration ([K
⫹
]) reflects total
body potassium stores at the steady state, although
this relationship can be disturbed in disorders of po-
tassium distribution (8). Plasma [K
⫹
] is a major de-
terminant of the resting potential of all cells (9). Hy-
perkalemia and hypokalemia are silent yet fatal
disturbances because of their arrhythmogenic poten-
tials (9). Insulin was shown to be an important regu-
lator of potassium homeostasis shortly after its dis-
covery (10). Basal insulin maintains fasting plasma
[K
⫹
] within the normal range (11). When insulin lev-
els are suppressed, plasma [K
⫹
] rises and pronounced
hyperkalemia develops after a potassium load (11).
Potassium is a well proven insulin secretagogue in the
intact organism and the isolated pancreas (12,13). In-
sulin is a key defender against exogenous potassium
load by using intracellular buffering to minimize hy-
perkalemia before renal excretion (14).
Hyperkalemia is often encountered in patients with
diabetes (8). The insulin-deficient state in type 1 dia-
betes predisposes to hyperkalemia because of an im-
paired ability of potassium to enter cells. During hy-
perglycemic hypertonic states in type 1 and type 2
diabetics, potassium is carried out of cells by convec-
tive flux as the most abundant intracellular cation
(15,16). Even at the steady state in a significant por-
tion of type 1 and type 2 diabetics, there is an im-
paired ability of the distal nephron to excrete potas-
sium because of hyporeninemic hypoaldosteronism
or tubular insensitivity to aldosterone (17,18). Finally,
one wonders whether there is impaired cellular po-
tassium uptake in type 2 diabetes as part of a gener-
alized insulin-resistant state.
One ponders whether there should be any teleogic
reasons of coupling glucose to potassium uptake. In
*The Charles and Jane
Pak Center for Mineral
Metabolism and
Clinical Research,
Departments of
†
Internal Medicine and
‡
Physiology, University
of Texas Southwestern
Medical Center, Dallas,
Texas
Correspondence: Orson
W. Moe, University of
Texas Southwestern
Medical Center, 5323
Harry Hines Boulevard,
Dallas, TX 75390-8885.
Phone: 214-648-7993;
Fax: 214-648-2526;
E-mail: orson.moe@
utsouthwestern.edu
www.cjasn.org Vol 6 July, 2011 Copyright © 2011 by the American Society of Nephrology 1533
Article
the postprandial state of herbivores or carnivores, caloric
and potassium influx are concurrent. In a feast-or-famine
situation in hunting carnivores, the magnitude of the load
is much exaggerated. The simultaneous shift of glucose
and potassium into cells makes physiologic sense with the
postprandial outpouring of insulin. Similarly, dietary
phosphate frequently accompanies caloric intake, and
upon entry into cells, glucose is phosphorylated; thus,
simultaneous phosphate uptake also makes physiologic
sense. However, if potassium, phosphate, and glucose
loads are applied discordantly, the simultaneous cellular
uptake will clearly present a homeostatic quandary and
some means of dissociation is mandatory.
Previous studies have addressed whether potassium
and glucose uptake are coupled. DeFronzo et al. observed
a relationship between the decline in plasma [K
⫹
] and
insulin level as well the total amount of glucose taken up
by cells (19). Arslanian et al. concluded that insulin-depen-
dent diabetics have impaired potassium uptake (20). How-
ever, Cohen et al. found independent actions of insulin on
glucose and potassium uptake (21). Our study contains a
larger number of human subjects and intends to encom-
pass a wider range of “insulin sensitivity” comparing non-
diabetic to diabetic subjects. We conclude that glucose and
potassium uptake are differentially regulated and that im-
paired glucose disposal does not affect potassium uptake.
Materials and Methods
Subjects
There were 45 study subjects. The diagnosis of type 2
diabetes was made by the participants’ personal physicians
before enrollment on the basis of elevated fasting or ran-
dom serum glucose (ⱖ126 mg/dl or ⱖ200 mg/dl, respec-
tively) on two separate occasions. Nondiabetics included
subjects with a broad range of body mass indices (BMIs)
without a known history of type 2 diabetes that was con-
firmed by a fasting glucose of ⬍126 mg/dl (highest value
was 106 mg/dl). Diabetic subjects were excluded if they
were treated with insulin and/or thiazolidinediones.
Treatment included metformin alone (n⫽6), a sulfonyl
urea alone (n⫽2), metformin and sulfonyl urea (n⫽3), or
diet alone (n⫽2). The Institutional Review Board at the
University of Texas Southwestern Medical Center ap-
proved the study, and all participants provided informed
consent. All subjects consumed a fixed metabolic diet for 8
days as outpatients for the first 5 days, and then as inpa-
tients for 3 days at the General Clinical Research Center at
University of Texas Southwestern Medical Center starting
on the evening of the 5th day. On the evening of day 8,
subjects fasted overnight except for 300 ml of water at
bedtime.
Hyperinsulinemic Euglycemic Insulin Clamp Technique
On day 9, breakfast was withheld and subjects under-
went hyperinsulinemic euglycemic clamp (22) starting at
8:00 a.m. with insulin infusion at 80 mU/m
2
of body sur-
face area for 2 hours. A 20-g/dl glucose solution was
started after 4 minutes of insulin infusion to maintain
plasma glucose concentration at the fasting levels through-
out the clamp procedure. Plasma insulin was determined
by a modification of the method of Yallow and Berson
(23,24). Blood for plasma glucose levels was drawn every 5
minutes from an arterialized dorsal hand vein kept in a
hotbox at 70°C (25). A glucose analyzer (YSI, Yellow
Springs, OH) was used to measure plasma glucose, and the
rate of the glucose infusion was adjusted to maintain eu-
glycemia. Peripheral venous blood was drawn without
stasis from an antecubital vein for electrolytes and lipid
profile at 8:00 and 10:00 a.m. Two timed urine specimens
were collected between 6:00 and 8:00 a.m. (preclamp) and
8:00 and 10:00 a.m. (hyperinsulinemia). To ensure ade-
quate urinary output, 250 ml of water was given orally at
6:00 and 8:00 a.m. Urine was collected under mineral oil
and kept refrigerated until analysis. Plasma and urinary
electrolytes and plasma lipid profiles were measured by an
autoanalyzer (Beckman, Synchron CX9ALX, Brea, CA).
Calculations and Analytical Methods
Glucose disposal rate during the hyperinsulinemic
phase with complete suppression of gluconeogenesis and
glycogenolysis, and absence of glycosuria was calculated
as equivalent to the infusion rate of glucose from time 80 to
120 minutes. A fall in plasma [K
⫹
] or phosphate concen-
tration was defined as the level obtained at 8:00 a.m. minus
that obtained at 10:00 a.m. Instead of using the “potassium
clamp” described by Choi and co-workers, (26) we used a
balance approach because it is technically difficult to do
simultaneous glucose and potassium clamps. Cellular [K
⫹
]
or phosphate uptake was calculated by subtracting the
urinary excretion rate from the fall in extracellular potas-
sium or phosphate content during the clamp. Extracellular
fluid volume was calculated as 0.2 L/kg ⫻body weight in
kilograms. This method is more accurate than the decre-
ment in plasma [K
⫹
] but technically simpler than the po-
tassium clamp. Phosphorus uptake was similarly calcu-
lated as the difference between the fall in extracellular
phosphorus uptake and urinary phosphorus excretion.
Comparison between groups was evaluated using the t
test with a two-tailed Pvalue, and a paired ttest was used
for paired analyses. A
2
test was used to compare per-
centages between groups. The Pearson correlation coeffi-
cient was used to assess correlation between different pa-
rameters. Statistical analyses were performed with SAS
version 9.1.3 (SAS Institute, Cary, NC).
Results
Patient Characteristics
The diabetic and nondiabetic groups were similar in age,
gender, gender race, cholesterol, and basal creatinine levels
(Table 1). Mean BMI was in the obese range for the diabetic
group and in the overweight range for the nondiabetic
group. There was also a higher percentage of Hispanics in
the diabetic than the nondiabetic group. In addition, the
diabetic group had a lower LDL, lower HDL, higher tri-
glyceride, and higher fasting glucose than the nondiabetic
group.
Plasma and Urinary Chemistry
The diabetic group had a numerically higher preclamp
plasma insulin level than the nondiabetic group, but the
difference was not statistically significant (12.0 ⫾8.4 versus
8.6 ⫾3.6
U/ml, P⫽0.25) (Table 2). The diabetic group
1534 Clinical Journal of the American Society of Nephrology
had higher preclamp (118 ⫾34 versus 92 ⫾7 mg/dl, P⫽
0.02) and postclamp (100 ⫾15 mg/dl versus 91 ⫾7 mg/dl,
P⫽0.05) glucose concentrations than the nondiabetic
group. There were no differences in serum creatinine, po-
tassium, and phosphate levels between the two groups
before and after insulin.
Glucose, Potassium, and Phosphate Uptake
There was a great deal of overlap of glucose disposal rate
between the two groups of subjects (Table 3). Type 2 dia-
betics have numerically lower glucose disposal rates than
nondiabetics (19.4 ⫾9.5 versus 26.1 ⫾13.2
mol/kg per
min, P⫽0.10). This is not surprising because the absolute
segregation of subjects into two distinct groups is artificial.
It is more meaningful to use a continuous independent
variable such as BMI as a surrogate. As expected, glucose
disposal rate falls as BMI rises when the two groups are
analyzed together (Figure 1A). In contrast, potassium (Fig-
ure 1B) and phosphate (Figure 1C) uptake do not correlate
at all with BMI. The fall in plasma [K
⫹
] was similar be-
tween the diabetic and nondiabetic groups (0.5 ⫾0.2 versus
0.5 ⫾0.3 mM, P⫽0.90). There were also no differences in
potassium uptake (72.2 ⫾37.8 versus 66.8 ⫾53.5 nmol/kg
per min, P⫽0.74) or phosphate uptake (40.9 ⫾24.3 versus
Table 1. Patient characteristics
Characteristics Nondiabetic Group Diabetic Group P
Number of patients 32 13
Age (years) 51 ⫾12 53 ⫾9 0.72
Percent male 59.4% 53.8% 0.73
Height (cm) 168 ⫾11 173 ⫾12 0.17
Weight (kg) 84 ⫾25 96 ⫾16 0.12
BMI (kg/m
2
)29.5 ⫾6.6 32.1 ⫾3.8 0.10
Race (%)
Caucasian 78.1% 76.9% 0.76
African American 18.8% 23.1% 0.93
Asian 3.1% 0.0%
Hispanic 6.3% 23.1% 0.27
non-Hispanic 93.8% 76.9% 0.27
Serum creatinine (mg/dl) 0.9 ⫾0.2 0.9 ⫾0.2 0.95
Creatinine clearance (ml/min) 116.7 ⫾27.9 121.0 ⫾22.8 0.62
LDL cholesterol (mg/dl) 132 ⫾36 106 ⫾38 0.04
Total cholesterol (mg/dl) 200 ⫾38 187 ⫾52 0.36
HDL cholesterol (mg/dl) 40 ⫾11 36 ⫾6 0.07
Triglyceride (mg/dl) 136 ⫾65 225 ⫾174 0.02
Glucose (mg/dl) 92 ⫾7 118 ⫾34 0.02
Hemoglobin A1c (%) 5.2 ⫾0.3 6.1 ⫾0.7 ⬍0.01
Values are mean ⫾standard deviation. BMI, body mass index.
Table 2. Serum and urine data before and after clamp
Data Preclamp/Postclamp Nondiabetic
Group Diabetic
Group P
Plasma [K
⫹
] (mM) Preclamp 4.0 ⫾0.4 4.0 ⫾0.2 0.58
Postclamp 3.5 ⫾0.2
a
3.6 ⫾0.3
a
0.41
Plasma phosphorus concentration (mM) Preclamp 0.93 ⫾0.11 1.00 ⫾0.16 0.11
Postclamp 0.57 ⫾0.11
b
0.69 ⫾0.19
b
0.05
Plasma creatinine (mg/dl) Preclamp 0.9 ⫾0.2 0.9 ⫾0.2 0.95
Postclamp 0.9 ⫾0.2 0.9 ⫾0.2 0.70
Plasma insulin (
U/ml) Preclamp 8.6 ⫾3.6 12.0 ⫾8.4 0.25
Postclamp 149.3 ⫾34.1
b
151.6 ⫾36.2
b
0.85
Plasma glucose (mg/dl) Preclamp 92 ⫾7 118 ⫾34 0.02
Postclamp 91 ⫾7 100 ⫾15 0.05
U
K
V (mmol/2 h) Preclamp 1.11 ⫾0.90 0.70 ⫾0.86 0.17
Postclamp 1.24 ⫾0.71 0.67 ⫾0.56 0.02
U
P
V (mmol/2 h) Preclamp 3.17 ⫾3.18 3.53 ⫾5.54 0.83
Postclamp 1.67 ⫾1.12
b
1.41 ⫾0.97 0.48
Values are mean ⫹/⫺standard deviation. [K
⫹
], potassium concentration; U
K
V, urine potassium excretion rate; U
P
V, urine
phosphorus excretion rate.
Pvalue compares nondiabetic group to diabetic group. Comparison of pre- versus postclamp values:
a
P⬍0.05,
b
P⬍0.01.
Clin J Am Soc Nephrol 6: 1533–1539, July, 2011 Glucose versus K
ⴙ
Regulation by Insulin, Nguyen et al. 1535
44.3 ⫾22.7 nmol/kg per min, P⫽0.65) rate between the
diabetic and nondiabetic groups. Despite the fall in glucose
disposal rate with increasing BMI, there was no relationship
between rate of potassium uptake (Figure 2A) or phosphate
uptake (Figure 2B) to glucose disposal rate, and there was no
correlation between potassium and phosphate uptake.
Discussion
Insulin shifts glucose and potassium from the extracel-
lular to the intracellular compartment. The primary goal of
this study was to examine whether these are coupled ac-
tions using subjects with a wide range of glucose disposal
rates. There was no correlation between potassium uptake
and BMI and between glucose disposal rate and the fall in
plasma [K
⫹
] or potassium uptake. A similar lack of rela-
tionship is observed with phosphate. This indicates that
the actions of insulin on glucose and potassium or phos-
phate uptake are independently regulated.
Classic physiologic studies in animals and humans sup-
port dissociative regulation. Potassium and sodium move-
ment in the isolated diaphragm in response to insulin
occurs in the absence of glucose (27). There is temporal
separation of potassium and glucose uptake (28,29), and
insulin stimulates potassium uptake in doses at which
there is no appreciable glucose flux (30). Rats fed a high-fat
diet developed slower uptake of glucose and potassium,
creating an apparent view of concordant regulation (31).
However, the high-fat diet resulted in a dramatically lower
potassium ingestion, which is likely the reason for the
reduction of cellular potassium buffering. When the high-
fat diet was supplemented with higher potassium to neu-
tralize the reduction in dietary potassium, cellular potas-
sium uptake was not different than control. This is strong
evidence to support discordant regulation.
Limited human studies have been performed. Hyperin-
sulinemic euglycemic clamps performed on 20 adolescents
with insulin-dependent diabetes and 10 age-matched con-
trols disclosed a slightly lower insulin-induced fall in
plasma [K
⫹
] in diabetic subjects and a correlation between
glucose disposal rate and fall in serum [K
⫹
] in control but
not in diabetic subjects (20). It is unclear why this relation-
ship is not maintained in diabetics if cell entry of glucose
and potassium are coupled. Patients with acanthosis nig-
ricans and insulin resistance have reduced glucose dis-
posal rate, but the fall in plasma [K
⫹
] was not affected (21).
DeFronzo et al. studied 29 normal nondiabetic subjects and
analyzed the potassium and glucose balance in the
splanchnic bed and the periphery (19). This study is cited
(20) to support concordant glucose and potassium uptake
by cells because of the positive correlation of the fall in
plasma [K
⫹
] (which is a composite of splanchnic and pe-
ripheral potassium transport) with glucose utilization.
Note that the DeFronzo study separately examined
splanchnic and peripheral potassium handling, which are
both very complex; in fact, the authors concluded that
there was no evidence in either system that potassium
uptake is coupled to glucose uptake (19).
We studied a larger number of human subjects with a
wide range of glucose disposal rates, including subjects
with high BMIs and some features of the metabolic
syndrome to frank type 2 diabetics, and showed clear
dissociation of glucose disposal from potassium uptake.
We also examined phosphate, which is another electro-
lyte for which the shift is regulated by insulin but the
cellular mechanisms are not defined (32,33). Because the
utilization of glucose mandates its conversion to glu-
cose-6-phosphate, concomitant stoichiometrically equiv-
alent coupled phosphate uptake into the same cells
seems logical. The interpretation of phosphate flux is
more complex because the fall in plasma phosphate
triggers a rapid secondary renal retention (34). This can
be due to the effect of falling plasma phosphate concen-
tration or a direct effect of insulin on the tubule (35). But
even correcting for this, we still did not observe a cor-
relation between glucose and phosphate uptake, further
suggesting that transport of different solutes are differ-
entially regulated by insulin.
Insulin receptor binding initiates a complicated cascade
eventuating in translocation of the facilitative glucose
transporter GLUT4 to the plasma membrane to affect glu-
cose uptake (36). Insulin stimulates potassium cellular up-
take by elevation and increased sensitivity to intracellular
sodium, translocation and activation Na
⫹
/K
⫹
-ATPase,
and inhibition of potassium efflux (30,37–43). The mecha-
nism of insulin-stimulated phosphate uptake is unknown.
It is clear that insulin receptor activation leads to divergent
glucose and potassium regulatory pathways, allowing
them to be independently regulated at a postreceptor level.
The postreceptor defect described in patients with the met-
abolic syndrome or type 2 diabetes mellitus affects the arm,
leading to glucose uptake but not potassium uptake. An
alternative and rather different view is that the reduction
of glucose uptake is a physiologic adaptive mechanism in
which the cells protect themselves against caloric overload
Table 3. Cellular uptakes and urinary excretion rates during hyperinsulinemia for three solutes in nondiabetic versus diabetic group
Nondiabetic Group Diabetic Group P
Glucose disposal rate (
mol/kg per min) 26.1 ⫾13.2 19.4 ⫾9.5 0.10
Change in plasma [K
⫹
] (mM) ⫺0.5 ⫾0.3 ⫺0.5 ⫾0.2 0.90
Potassium uptake (nmol/kg per min) 66.8 ⫾53.5 72.2 ⫾37.8 0.74
Change in U
K
V (mmol/2 h) 0.13 ⫾1.05 ⫺0.025 ⫾0.94 0.65
Change in plasma phosphorus concentration (mM) ⫺0.37 ⫾0.12 ⫺0.32 ⫾0.12 0.21
Phosphate uptake (nmol/kg per min) 44.3 ⫾22.7 40.9 ⫾24.3 0.65
Change in U
P
V (mmol/2 h) ⫺1.50 ⫾3.00 ⫺2.12 ⫾5.80 0.72
Values are mean ⫹/⫺standard deviation. [K], potassium concentration; U
K
V, urine potassium excretion rate; U
P
V, urine
phosphorus excretion rate.
1536 Clinical Journal of the American Society of Nephrology
and appropriately and specifically downregulate the glu-
cose uptake pathway (44). In this model, there will be no
reason to restrict entry of other solutes that do not bear
calories. Finally, insulin resistance may affect glucose and
potassium because serum [K
⫹
]per se may exert an effect on
insulin-induced potassium uptake (43), and any distur-
bance in serum [K
⫹
] may self-rectify the defect.
In addition to providing further foundation to search
for the underlying mechanisms and reasons for this
divergent regulation, there are some clinical implica-
tions. When treating hyperkalemia, insulin remains ef-
ficacious in diabetics and nondiabetics and one does not
need to resort to b-agonists, and diabetics do not require
different doses of insulin to shift potassium. Because the
commonly encountered “insulin-resistant” patients ac-
tually have preserved insulin-induced potassium dis-
posal, one wonders why their high insulin levels are not
causing hypokalemia. This remains to be explored, but it
is conceivable that any disturbance in serum [K
⫹
]is
capable of regulating insulin-stimulated potassium up-
A
B
C
Figure 1. |Relationship of (A) glucose, (B) potassium, and (C) phos-
phate uptake as a function of body mass index (BMI). Forty-five
subjects with a wide range of BMIs underwent hyperinsulinemic
euglycemic clamp. Glucose disposal rate was calculated from the
glucose infusion required to maintain euglycemia. Potassium and
phosphate uptake were calculated as the reduction in extracellular
potassium or phosphate corrected for urinary excretion. The corre-
lation coefficient was calculated for the relationship between the x
and yvalues as well as the Pvalue for the R
2
.
A
B
C
Figure 2. |Relationship between uptake of three solutes: (A) potas-
sium versus glucose, (B) phosphate versus glucose, and (C) phos-
phate versus potassium. Forty-five subjects with a wide range of
BMIs underwent hyperinsulinemic euglycemic clamp. Glucose dis-
posal rate was calculated from the glucose infusion required to
maintain euglycemia. Potassium and phosphate uptake were calcu-
lated as the reduction in extracellular potassium or phosphate corrected
for urinary excretion. The correlation coefficient was calculated for the
relationship between the xand yvalues as well as the Pvalue for the R
2
.
Clin J Am Soc Nephrol 6: 1533–1539, July, 2011 Glucose versus K
ⴙ
Regulation by Insulin, Nguyen et al. 1537
take (43). Our study confirms that insulin independently
regulates glucose and potassium uptake into cells and
this independence explains why in noninsulin-depen-
dent diabetic insulin resistance leads to impaired insulin
uptake into cells but has no effect on the cell’s potassium
disposal.
Acknowledgments
This work was supported by the National Institutes of Health
(M01-RR00633, P01-DK20543, R01-DK081423, and K23-RR21710),
the Charles Pak and Donald Seldin Endowment for Metabolic
Research, and the Simmons Family Foundation. We are grateful to
the expertise of Mr. John Poindexter for biostatistical support, the
nursing staff of the University of Texas Southwestern General
Clinical Research Center, and the technical staff at the Mineral
Metabolism Clinical Laboratory.
Disclosures
None.
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Received: January 26, 2011 Accepted: March 28, 2011
Published online ahead of print. Publication date available at
www.cjasn.org.
See related editorial, “A Critically Swift Response: Insulin-
Stimulated Potassium and Glucose Transport in Skeletal
Muscle,” on pages 1513–1516.
Clin J Am Soc Nephrol 6: 1533–1539, July, 2011 Glucose versus K
ⴙ
Regulation by Insulin, Nguyen et al. 1539
