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Effects of Pregnancy on Metabolism

Michael P. Diamond, Gabriele Rossi

10.1002/cphy.cp070231

Source: Supplement 21: Handbook of Physiology, The Endocrine System, The Endocrine Pancreas and Regulation of Metabolism

Originally published: 2001

Published online: January 2011

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Prepregnancy Period
2 First Trimester
2.1 Introduction
2.2 Carbohydrate Metabolism
2.3 Lipid Metabolism
2.4 Protein Metabolism
3 Second and Third Trimesters
4 Counterregulation During Pregnancy
Figure 1. Figure 1.

Comparison of insulin concentrations, glucose levels (a), and the rates of hepatic glucose production (b), and glucose utilization (c), both basically and during a two‐step (0.25 mU insulin/kg/min and 1.0 mU insulin/kg/min) euglycemic, hyperinsulinemic clamp in the follicular and luteal phases of the menstrual cycle in regularly menstruating women.

(Reprinted from Diamond MP, Jacob R, Connolly‐Diamond M, DeFronzo RA. Glucose metabolism during the menstrual cycle. j. Reprod. Med. 38:417–421, 1993.)
Figure 2. Figure 2.

Comparison of insulin concentrations, glucose levels (a), and the rates of hepatic glucose production (b), and glucose utilization (c), both basically and during a two‐step (0.25 mU insulin/kg/min and 1.0 mU insulin/kg/min) euglycemic, hyperinsulinemic clamp in the follicular and luteal phases of the menstrual cycle in regularly menstruating women.

(Reprinted from Diamond MP, Jacob R, Connolly‐Diamond M, DeFronzo RA. Glucose metabolism during the menstrual cycle. j. Reprod. Med. 38:417–421, 1993.)
Figure 3. Figure 3.

Hyperglycemic clamp (= 125 mg/dk) glucose uptake (M) (left) and ratio of glucose uptake to insulin response (M, ratio) (right) in the follicular and luteal phases of the menstrual cycle in eight women. Data displayed represent individual levels of each woman and mean levels in each phase of the cycle.

(Reprinted from Diamond MP, Simonson DC, DeFronzo RA. Menstrual cyclicity has a profound effect on glucose homeostasis. Fertil Steril Vol. 62 (2), 204–208, 1989).
Figure 4. Figure 4.

Rates of glucose uptake in seven patients with premenstrual hyperglycemia (group J, open bars) and nine patients without premenstrual hyperglycemia (group 2, shaded bars) during follicular and luteal phases of menstrual cycle. Data are expressed as means ± SE.

(Reprinted from Widom B, Diamond MP, Simonson DC. Alterations in glucose metabolism during menstrual cycle in women with IDDM. Diabetes 15:213–220, 1992.)
Figure 5. Figure 5.

Stages of development at time of recovery and after culture of embryos recovered from (a) nondiabetic control mice (n = 464) and streptozotocin‐diabetic mice (n = 387), and (b) nondiabetic control mice (n = 252) and alloxan‐diabetic mice (n = 224). Embryo development was graded as degenerated (Deg), 2‐cell 2, 3‐cell 3, 4‐cell 4, 6‐cell 6, 8‐cell 8, morula (M), blastocyst (B), and expanded blastocyst (EB).

(Reprinted from Diamond MP, Moley KH, Pellicer A, Vaughn WK, DeCherney AH. Effects of streptozotocin and alloxan‐induced diabetes mellitus on mouse follicular and early embryo development. J. Reprod. Fertil. 86:1–10, 1989.)
Figure 6. Figure 6.

Distribution of developmental stages (a) at a time of recovery and after (b) 24, (c) 48 or (d) 72 h of in‐vitro culture of pre‐implantation embryos recovered from nondiabetic F1 hybrid mice (□; 17 mice, 175 embryos) nondiabetic NOD mice (□; 7 mice, 81 embryos) diabetic NOD mice (▪; 9 mice, 68 embryos) and diabetic NOD mice treated with insulin (□; 7 mice, 71 embryos).

(Reprinted from Moley KH, Vaughn WK, DeCherney AH, Diamond MP. Effects of diabetes on mouse pre‐implantation embryo development. J. Reprod. Fertil. 93:325–332, 1991.)
Figure 7. Figure 7.

Glucose uptake and clearance during euglycemic hyperinsulinemic clamp studies. Values are means ± SE for samples collected at 10 min intervals over final 30 min of basal and insulin infusion periods. “P < 0.05 vs. Value in control group.

(Reprinted from Rossi G, Sherwin RS, Penzias AS, Lapaczewski P, Jacob RJ, Shulman GI, Diamond MP. Temporal changes in insulin resistance and secretion in 24‐h fasted conscious pregnant rats. Am J. Physiol. E845–E851, Dec. 1993.)
Figure 8. Figure 8.

Endogenous glucose production during euglycemic hyperinsulinemic clamp studies. Rates of glucose production during basal period and over final 30 min of insulin infusion periods are plotted as function of steady‐state plasma insulin levels. In late pregnant animals, data are presented from both 9/45 and 12/60 pmol·kg−1 min−1 studies. Values are means ± SE.

(Reprinted from Rossi G, Sherwin RS, Penzias AS, Lapaczewski P, Jacob RJ, Shulman GI, Diamond MP. Temporal changes in insulin resistance and secretion in 24‐h fasted conscious pregnant rats. Am J. Physiol. E845–E851, Dec. 1993.)
Figure 9. Figure 9.

Plasma glucose levels during hypoglycemic clamp studies in pregnant, intensively treated insulin‐dependent diabetic women; and nonpregnant, nondiabetic control women.

(From Diamond MP, Reece EA, Caprio S, et al. Impairment of counter regulatory hormone responses to hypoglycemia in pregnant women with insulin‐dependent diabetes mellitus.)
Figure 10. Figure 10.

Epinephrine, norepinephrine, and glucagon responses to hypoglycemia in pregnant, intensively treated insulin‐dependent diabetic women, and nonpregnant, nondiabetic control women.

(From Diamond MP, Reece EA, Caprio S, et al. Impairment of counter regulatory hormone respones to hypoglycemia in pregnant women with insulin‐dependent diabetes mellitus.)
Figure 11. Figure 11.

Changes in growth hormone and cortisol levels from basal concentrations during hypoglycemic clamp studies in pregnant, intensively treated insulin‐dependent diabetic women, and nonpregnant, nondiabetic control women.

(From Diamond MP, Reece EA, Caprio S, et al. Impairment of counter regulatory hormone responses to hypoglycemia in pregnant women with insulin‐dependent diabetes mellitus.)
Figure 12. Figure 12.

Human chorionic gonadotropin and hPL levels in pregnant, intensively treated insulin‐dependent diabetic women during hypoglycemic clamp studies.

(From Diamond MP, Reece EA, Caprio S, et al. Impairment of counter regulatory hormone responses to hypoglycemia in pregnant women with insulin‐dependent diabetes mellitus.)


Figure 1.

Comparison of insulin concentrations, glucose levels (a), and the rates of hepatic glucose production (b), and glucose utilization (c), both basically and during a two‐step (0.25 mU insulin/kg/min and 1.0 mU insulin/kg/min) euglycemic, hyperinsulinemic clamp in the follicular and luteal phases of the menstrual cycle in regularly menstruating women.

(Reprinted from Diamond MP, Jacob R, Connolly‐Diamond M, DeFronzo RA. Glucose metabolism during the menstrual cycle. j. Reprod. Med. 38:417–421, 1993.)


Figure 2.

Comparison of insulin concentrations, glucose levels (a), and the rates of hepatic glucose production (b), and glucose utilization (c), both basically and during a two‐step (0.25 mU insulin/kg/min and 1.0 mU insulin/kg/min) euglycemic, hyperinsulinemic clamp in the follicular and luteal phases of the menstrual cycle in regularly menstruating women.

(Reprinted from Diamond MP, Jacob R, Connolly‐Diamond M, DeFronzo RA. Glucose metabolism during the menstrual cycle. j. Reprod. Med. 38:417–421, 1993.)


Figure 3.

Hyperglycemic clamp (= 125 mg/dk) glucose uptake (M) (left) and ratio of glucose uptake to insulin response (M, ratio) (right) in the follicular and luteal phases of the menstrual cycle in eight women. Data displayed represent individual levels of each woman and mean levels in each phase of the cycle.

(Reprinted from Diamond MP, Simonson DC, DeFronzo RA. Menstrual cyclicity has a profound effect on glucose homeostasis. Fertil Steril Vol. 62 (2), 204–208, 1989).


Figure 4.

Rates of glucose uptake in seven patients with premenstrual hyperglycemia (group J, open bars) and nine patients without premenstrual hyperglycemia (group 2, shaded bars) during follicular and luteal phases of menstrual cycle. Data are expressed as means ± SE.

(Reprinted from Widom B, Diamond MP, Simonson DC. Alterations in glucose metabolism during menstrual cycle in women with IDDM. Diabetes 15:213–220, 1992.)


Figure 5.

Stages of development at time of recovery and after culture of embryos recovered from (a) nondiabetic control mice (n = 464) and streptozotocin‐diabetic mice (n = 387), and (b) nondiabetic control mice (n = 252) and alloxan‐diabetic mice (n = 224). Embryo development was graded as degenerated (Deg), 2‐cell 2, 3‐cell 3, 4‐cell 4, 6‐cell 6, 8‐cell 8, morula (M), blastocyst (B), and expanded blastocyst (EB).

(Reprinted from Diamond MP, Moley KH, Pellicer A, Vaughn WK, DeCherney AH. Effects of streptozotocin and alloxan‐induced diabetes mellitus on mouse follicular and early embryo development. J. Reprod. Fertil. 86:1–10, 1989.)


Figure 6.

Distribution of developmental stages (a) at a time of recovery and after (b) 24, (c) 48 or (d) 72 h of in‐vitro culture of pre‐implantation embryos recovered from nondiabetic F1 hybrid mice (□; 17 mice, 175 embryos) nondiabetic NOD mice (□; 7 mice, 81 embryos) diabetic NOD mice (▪; 9 mice, 68 embryos) and diabetic NOD mice treated with insulin (□; 7 mice, 71 embryos).

(Reprinted from Moley KH, Vaughn WK, DeCherney AH, Diamond MP. Effects of diabetes on mouse pre‐implantation embryo development. J. Reprod. Fertil. 93:325–332, 1991.)


Figure 7.

Glucose uptake and clearance during euglycemic hyperinsulinemic clamp studies. Values are means ± SE for samples collected at 10 min intervals over final 30 min of basal and insulin infusion periods. “P < 0.05 vs. Value in control group.

(Reprinted from Rossi G, Sherwin RS, Penzias AS, Lapaczewski P, Jacob RJ, Shulman GI, Diamond MP. Temporal changes in insulin resistance and secretion in 24‐h fasted conscious pregnant rats. Am J. Physiol. E845–E851, Dec. 1993.)


Figure 8.

Endogenous glucose production during euglycemic hyperinsulinemic clamp studies. Rates of glucose production during basal period and over final 30 min of insulin infusion periods are plotted as function of steady‐state plasma insulin levels. In late pregnant animals, data are presented from both 9/45 and 12/60 pmol·kg−1 min−1 studies. Values are means ± SE.

(Reprinted from Rossi G, Sherwin RS, Penzias AS, Lapaczewski P, Jacob RJ, Shulman GI, Diamond MP. Temporal changes in insulin resistance and secretion in 24‐h fasted conscious pregnant rats. Am J. Physiol. E845–E851, Dec. 1993.)


Figure 9.

Plasma glucose levels during hypoglycemic clamp studies in pregnant, intensively treated insulin‐dependent diabetic women; and nonpregnant, nondiabetic control women.

(From Diamond MP, Reece EA, Caprio S, et al. Impairment of counter regulatory hormone responses to hypoglycemia in pregnant women with insulin‐dependent diabetes mellitus.)


Figure 10.

Epinephrine, norepinephrine, and glucagon responses to hypoglycemia in pregnant, intensively treated insulin‐dependent diabetic women, and nonpregnant, nondiabetic control women.

(From Diamond MP, Reece EA, Caprio S, et al. Impairment of counter regulatory hormone respones to hypoglycemia in pregnant women with insulin‐dependent diabetes mellitus.)


Figure 11.

Changes in growth hormone and cortisol levels from basal concentrations during hypoglycemic clamp studies in pregnant, intensively treated insulin‐dependent diabetic women, and nonpregnant, nondiabetic control women.

(From Diamond MP, Reece EA, Caprio S, et al. Impairment of counter regulatory hormone responses to hypoglycemia in pregnant women with insulin‐dependent diabetes mellitus.)


Figure 12.

Human chorionic gonadotropin and hPL levels in pregnant, intensively treated insulin‐dependent diabetic women during hypoglycemic clamp studies.

(From Diamond MP, Reece EA, Caprio S, et al. Impairment of counter regulatory hormone responses to hypoglycemia in pregnant women with insulin‐dependent diabetes mellitus.)
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Article Title: Effects of Pregnancy on Metabolism
 

How to Cite

Michael P. Diamond, Gabriele Rossi. Effects of Pregnancy on Metabolism. Compr Physiol 2011, Supplement 21: Handbook of Physiology, The Endocrine System, The Endocrine Pancreas and Regulation of Metabolism: 951-968. First published in print 2001. doi: 10.1002/cphy.cp070231