AACE ePoster Library

COMPENSATORY PANCREATIC β-CELL FUNCTION IN HEALTHY NORMOGLYCEMIC MEN MODIFIES BUT DOES NOT FULLY CORRECT THE DISRUPTED GLUCOSE HOMEOSTASIS INDUCED BY INCREASING BODY FAT IN FASTING AND FED STATES
AACE ePoster Library. Lawson D. 05/13/15; 97766; 602
Dr. Donna Lawson
Dr. Donna Lawson
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Abstract
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Objective: This study was intended to assess the glucose regulatory status in healthy men of variable total body fat
mass.
Methods: Eighty one men aged 18-78 years with BMIs of 18-39 kg/m² were studied on 2 randomly ordered occasions
after an overnight fast, followed by ingestion of either 75 grams of dextrose solution or equal volume of water.
Sessions started between the hrs of 0800-0900 and continued for 6.5 hrs, with blood collected at 10-min intervals for
the measurements of glucose and insulin. Adiponectin concentration was assayed in the first blood sample. Total
body fat was determined by DXA. Fat mass index (FMI: kg/m2) was calculated using total body fat (kg) and height
(m). Parameters of interest were fasting concentrations of glucose and insulin, mean and areas under the 6.5 hr
concentration time series (AUC), peak concentrations and time to peaks after dextrose ingestion. Linear regression
was used to relate hormone data to body-composition variables.
Results or Case Presentation: Regression analysis revealed significant positive correlation (r coefficient:P value)
between FMI and each of: FBG (0.26:0.017), 6.5 hrs water-day mean glucose (0.23:0.043) and AUC (0.22:0.047), 6.5
hr dextrose-day mean glucose (0.42:<0.0001) and AUC (0.42:<0.0001), post-dextrose peak glucose (0.42:0.0001),
and time to peak glucose (0.26:0.019). FMI also was positively correlated with insulin levels in the fasting state
(0.6:<0.0001), 6.5 hrs water-day mean (0.63:<0.0001) and AUC (0.64:<0.0001), 6.5 hr dextrose-day mean
(0.53:<0.0001) and AUC (0.53:<0.0001), and post-dextrose peak insulin (0.45:<0.0001) . Adiponectin had significant
negative correlation with FMI (-0.22:0.044).
Discussion: Increased body fat is known to induce insulin resistance, and increase β-cell insulin secretion. Such
compensatory mechanisms are believed to maintain initially normal glucose homeostasis. The present study identifies
altered glucose metabolism albeit within the normal range with increasing body fat, as characterized by relatively
higher blood glucose in the fasting state, and more pronounced increases in all measures of glucose concentrations
after dextrose ingestion, including peak and time to peak glucose levels.
Conclusion: Quantitatively impaired glucose disposal associated with increasing body fat in healthy men, despite
compensatory augmentation of β-cell function, identifies compromised glucose regulation, which could be inferred as
a precursor to the development of subclinical and clinical diabetes. Having a negative correlation with fat mass,
hypoadiponectineimia could be proposed as a contributory factor.
Objective: This study was intended to assess the glucose regulatory status in healthy men of variable total body fat
mass.
Methods: Eighty one men aged 18-78 years with BMIs of 18-39 kg/m² were studied on 2 randomly ordered occasions
after an overnight fast, followed by ingestion of either 75 grams of dextrose solution or equal volume of water.
Sessions started between the hrs of 0800-0900 and continued for 6.5 hrs, with blood collected at 10-min intervals for
the measurements of glucose and insulin. Adiponectin concentration was assayed in the first blood sample. Total
body fat was determined by DXA. Fat mass index (FMI: kg/m2) was calculated using total body fat (kg) and height
(m). Parameters of interest were fasting concentrations of glucose and insulin, mean and areas under the 6.5 hr
concentration time series (AUC), peak concentrations and time to peaks after dextrose ingestion. Linear regression
was used to relate hormone data to body-composition variables.
Results or Case Presentation: Regression analysis revealed significant positive correlation (r coefficient:P value)
between FMI and each of: FBG (0.26:0.017), 6.5 hrs water-day mean glucose (0.23:0.043) and AUC (0.22:0.047), 6.5
hr dextrose-day mean glucose (0.42:<0.0001) and AUC (0.42:<0.0001), post-dextrose peak glucose (0.42:0.0001),
and time to peak glucose (0.26:0.019). FMI also was positively correlated with insulin levels in the fasting state
(0.6:<0.0001), 6.5 hrs water-day mean (0.63:<0.0001) and AUC (0.64:<0.0001), 6.5 hr dextrose-day mean
(0.53:<0.0001) and AUC (0.53:<0.0001), and post-dextrose peak insulin (0.45:<0.0001) . Adiponectin had significant
negative correlation with FMI (-0.22:0.044).
Discussion: Increased body fat is known to induce insulin resistance, and increase β-cell insulin secretion. Such
compensatory mechanisms are believed to maintain initially normal glucose homeostasis. The present study identifies
altered glucose metabolism albeit within the normal range with increasing body fat, as characterized by relatively
higher blood glucose in the fasting state, and more pronounced increases in all measures of glucose concentrations
after dextrose ingestion, including peak and time to peak glucose levels.
Conclusion: Quantitatively impaired glucose disposal associated with increasing body fat in healthy men, despite
compensatory augmentation of β-cell function, identifies compromised glucose regulation, which could be inferred as
a precursor to the development of subclinical and clinical diabetes. Having a negative correlation with fat mass,
hypoadiponectineimia could be proposed as a contributory factor.

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