The Role of Hormones in Shaping Body Composition Throughout Pregnancy

Pregnancy is a unique physiological state in which the body undergoes profound hormonal remodeling to support fetal development, prepare for lactation, and protect maternal health. These hormonal shifts are the primary drivers behind the changes in body composition that occur throughout gestation. While the visible outcomes—such as weight gain and alterations in body shape—are often the focus of discussion, the underlying endocrine mechanisms are what truly dictate how and where the body stores or mobilizes energy, retains water, and remodels tissues. Understanding these hormonal pathways provides a solid foundation for clinicians, researchers, and expectant mothers who wish to grasp the biological basis of body‑composition changes during pregnancy.

The Hormonal Landscape of Pregnancy

From conception to delivery, a cascade of hormones is released by the ovaries, placenta, pituitary gland, adrenal cortex, and other endocrine organs. These hormones do not act in isolation; rather, they form an intricate network of feedback loops that modulate metabolism, appetite, fluid balance, and tissue remodeling. The most influential hormones in shaping body composition include:

• Estrogen – produced by the ovaries early in pregnancy and later by the placenta.
• Progesterone – secreted by the corpus luteum and placenta.
• Human Placental Lactogen (hPL) – a placenta‑derived hormone with strong metabolic effects.
• Prolactin – primarily from the anterior pituitary, preparing the breast for lactation.
• Relaxin – released by the corpus luteum and placenta, affecting connective tissue.
• Cortisol – adrenal hormone that rises progressively throughout gestation.
• Insulin and related pancreatic hormones – modulated by placental factors.
• Leptin and ghrelin – adipokines that regulate hunger and satiety.
• Thyroid hormones (T3, T4) – essential for basal metabolic rate.
• Growth hormone (GH) and insulin‑like growth factor‑1 (IGF‑1) – involved in tissue growth and protein synthesis.

Each of these agents contributes to a distinct aspect of body‑composition remodeling, from the expansion of adipose stores to the retention of extracellular fluid and the preservation of protein reserves.

Estrogen and Progesterone: Primary Drivers of Metabolic Reprogramming

Estrogen rises sharply after implantation and continues to increase, reaching peak concentrations in the third trimester. Its metabolic actions are multifaceted:

1. Lipogenesis Stimulation – Estrogen up‑regulates lipogenic enzymes (e.g., acetyl‑CoA carboxylase, fatty acid synthase) in subcutaneous adipose tissue, promoting the synthesis of triglycerides. This creates an energy reservoir that can be mobilized during late‑gestation fasting or early lactation.
2. Modulation of Lipolysis – By enhancing the expression of hormone‑sensitive lipase inhibitors, estrogen dampens basal lipolysis, ensuring that stored fat is not prematurely depleted.
3. Vascular Effects – Estrogen promotes vasodilation and increases capillary perfusion of adipose depots, facilitating nutrient delivery and storage.

Progesterone, which also climbs steadily throughout pregnancy, exerts complementary but distinct influences:

4. Insulin Antagonism – Progesterone reduces insulin sensitivity in peripheral tissues, shifting glucose utilization toward the fetus and encouraging the maternal body to store excess glucose as fat.
5. Protein Sparing – By attenuating muscle protein breakdown, progesterone helps preserve lean tissue, indirectly influencing the proportion of fat versus lean mass.
6. Fluid Retention – Progesterone stimulates the renin‑angiotensin‑aldosterone system (RAAS), leading to sodium and water retention that contributes to the overall increase in body mass.

Together, estrogen and progesterone establish a metabolic environment that favors energy storage, particularly in the form of subcutaneous fat, while protecting essential protein stores.

Human Placental Lactogen and Metabolic Adaptations

Human placental lactogen (hPL), also known as chorionic somatomammotropin, is a unique hormone secreted exclusively by the syncytiotrophoblast. Its concentration mirrors placental mass, peaking in the late second and early third trimesters. hPL’s primary metabolic actions include:

• Inducing Peripheral Insulin Resistance – hPL interferes with insulin signaling pathways in muscle and adipose tissue, ensuring that glucose remains available for transplacental transport.
• Promoting Lipolysis in Adipose Tissue – While estrogen suppresses basal lipolysis, hPL stimulates catecholamine‑mediated lipolysis, releasing free fatty acids (FFAs) into the maternal circulation. These FFAs become a crucial fuel source for the mother during periods of fasting, sparing glucose for the fetus.
• Enhancing Lipid Mobilization – hPL up‑regulates adipose triglyceride lipase (ATGL) and hormone‑sensitive lipase (HSL), facilitating the breakdown of stored triglycerides.

The net effect of hPL is a finely tuned balance: it encourages the accumulation of fat early in pregnancy (under estrogen’s influence) and later promotes the mobilization of that fat to meet the heightened energy demands of late gestation.

Prolactin and Energy Balance

Prolactin, best known for its role in lactogenesis, also participates in metabolic regulation during pregnancy:

• Appetite Stimulation – Prolactin receptors in the hypothalamus interact with neuropeptide Y (NPY) pathways, modestly increasing hunger signals.
• Adipocyte Differentiation – Prolactin can promote the differentiation of pre‑adipocytes into mature adipocytes, contributing to the expansion of adipose tissue.
• Glucose Homeostasis – By enhancing pancreatic β‑cell proliferation, prolactin supports increased insulin secretion, which counterbalances the insulin resistance induced by progesterone and hPL.

Thus, prolactin helps ensure that sufficient caloric intake accompanies the metabolic shifts that favor fat storage.

Relaxin and Connective Tissue Remodeling

Relaxin, a peptide hormone secreted by the corpus luteum and later by the placenta, is primarily recognized for its role in ligamentous laxity and cervical softening. However, its influence on body composition is indirect yet significant:

• Extracellular Matrix (ECM) Turnover – Relaxin stimulates matrix metalloproteinases (MMPs), facilitating the remodeling of connective tissue. This process allows adipose depots to expand more readily without compromising structural integrity.
• Fluid Distribution – By increasing vascular permeability, relaxin contributes to the redistribution of interstitial fluid, which can affect measured body mass and perceived “bloating.”

While relaxin does not directly alter macronutrient storage, its actions create a permissive environment for the physical expansion of adipose tissue and the accommodation of increased fluid volume.

Cortisol and Stress‑Related Metabolism

Maternal cortisol levels rise progressively throughout pregnancy, driven by increased production of corticotropin‑releasing hormone (CRH) from the placenta. Cortisol’s metabolic effects are pivotal for body‑composition dynamics:

• Gluconeogenesis Promotion – Cortisol stimulates hepatic glucose production, ensuring a steady supply of glucose for both mother and fetus.
• Protein Catabolism – In prolonged elevations, cortisol can increase proteolysis, particularly in skeletal muscle, releasing amino acids for fetal growth. However, the concurrent rise in progesterone mitigates excessive muscle loss.
• Lipolysis Enhancement – Cortisol synergizes with hPL to augment lipolysis, especially in visceral adipose stores, providing additional FFAs for maternal energy needs.

The balance between cortisol’s catabolic actions and the anabolic influences of estrogen and progesterone determines the net effect on maternal body composition.

Insulin Sensitivity and Pancreatic Hormones

Insulin dynamics undergo a biphasic shift during gestation:

1. Early Pregnancy – Insulin sensitivity is relatively preserved, allowing efficient glucose uptake.
2. Mid‑to‑Late Pregnancy – Hormones such as progesterone, hPL, and cortisol induce a state of insulin resistance, particularly in peripheral tissues.

To compensate, pancreatic β‑cells expand in both number and functional capacity, secreting higher amounts of insulin. This hyperinsulinemic response:

• Facilitates Glucose Storage – Excess glucose is directed toward hepatic glycogen synthesis and adipose lipogenesis.
• Preserves Fetal Glucose Supply – By limiting maternal peripheral glucose utilization, more glucose remains available for placental transfer.

The interplay between insulin resistance and compensatory hyperinsulinemia is central to the accumulation of maternal fat stores.

Leptin, Ghrelin, and Appetite Regulation

Adipose tissue itself becomes an endocrine organ during pregnancy, secreting leptin and influencing ghrelin pathways:

• Leptin – Levels rise in proportion to fat mass and are further amplified by placental production. Elevated leptin signals satiety to the hypothalamus, yet pregnancy is characterized by a relative leptin resistance, allowing increased caloric intake despite high leptin concentrations.
• Ghrelin – The hunger‑stimulating hormone may be suppressed by rising estrogen and progesterone, but the net effect of leptin resistance and prolactin‑mediated appetite stimulation often results in a modest increase in food consumption.

These hormonal adjustments ensure that energy intake aligns with the heightened metabolic demands of gestation.

Thyroid Hormones and Basal Metabolic Rate

Thyroid function is subtly altered in pregnancy:

• Increased Total T4 and T3 – Elevated estrogen raises thyroid‑binding globulin (TBG), increasing total circulating thyroid hormones while free hormone levels remain relatively stable.
• Enhanced Basal Metabolic Rate (BMR) – The modest rise in free T3 contributes to a higher BMR, supporting the increased energy expenditure associated with fetal growth and maternal tissue expansion.

Adequate thyroid hormone availability is essential for maintaining the metabolic flexibility required for body‑composition changes.

Growth Hormone and the IGF Axis

Maternal growth hormone (GH) and placental growth hormone (PGH) together shape the insulin‑like growth factor (IGF) system:

• PGH Dominance – By the second trimester, PGH replaces pituitary GH as the primary GH in circulation, stimulating hepatic production of IGF‑1.
• Anabolic Effects – IGF‑1 promotes protein synthesis and modestly supports lean‑tissue accretion, while also enhancing lipogenesis in adipose tissue.
• Nutrient Partitioning – The GH/IGF axis helps allocate nutrients between maternal stores and fetal growth, influencing the proportion of fat versus protein retained in the mother.

Although the contribution of GH to overall weight gain is smaller than that of estrogen or progesterone, its role in fine‑tuning tissue composition is noteworthy.

Integrated Hormonal Interactions: A Systems Perspective

The hormonal milieu of pregnancy functions as a highly coordinated system rather than a collection of isolated signals. Key integrative concepts include:

• Feedback Loops – For example, rising leptin normally suppresses appetite, but estrogen‑induced leptin resistance blunts this feedback, allowing increased caloric intake.
• Synergistic Lipid Metabolism – Estrogen’s lipogenic drive combined with hPL‑mediated lipolysis creates a dynamic “store‑and‑release” mechanism that ensures a ready supply of FFAs while preserving glucose for the fetus.
• Temporal Shifts – Early gestation favors anabolic processes (fat storage, protein sparing), whereas late gestation tilts toward catabolic pathways (lipolysis, gluconeogenesis) to meet the energy demands of rapid fetal growth and preparation for lactation.
• Cross‑Organ Communication – The placenta acts as an endocrine hub, releasing hPL, relaxin, and PGH, which in turn modulate maternal liver, adipose tissue, muscle, and brain function.

Understanding these interconnections clarifies why body‑composition changes are not merely a matter of “eating more” but reflect a sophisticated hormonal orchestration.

Clinical Relevance and Monitoring

From a clinical standpoint, recognizing the hormonal drivers of body‑composition changes can inform:

• Risk Assessment – Excessive insulin resistance or abnormal cortisol elevation may predispose to gestational diabetes or hypertensive disorders, which in turn affect maternal adiposity.
• Targeted Interventions – While the article avoids specific nutrition strategies, clinicians can consider hormonal profiles when counseling patients about appropriate weight‑gain trajectories.
• Post‑partum Considerations – After delivery, abrupt declines in estrogen, progesterone, and hPL reverse many of the metabolic adaptations, often leading to rapid mobilization of stored fat. Understanding the hormonal basis helps anticipate and manage postpartum weight‑loss patterns.

Routine monitoring of fasting glucose, lipid panels, and, when indicated, cortisol or thyroid function tests can provide indirect insight into the hormonal status influencing body composition.

Summary and Key Takeaways

• Pregnancy triggers a coordinated surge of hormones—estrogen, progesterone, hPL, prolactin, relaxin, cortisol, insulin, leptin, ghrelin, thyroid hormones, and the GH/IGF axis—that collectively reshape maternal body composition.
• Early gestation is dominated by anabolic signals (estrogen‑driven lipogenesis, progesterone‑mediated protein sparing) that promote the accumulation of subcutaneous fat and fluid.
• Mid‑to‑late pregnancy introduces catabolic forces (hPL‑stimulated lipolysis, cortisol‑enhanced gluconeogenesis) that mobilize stored energy while preserving glucose for the fetus.
• Hormonal cross‑talk creates a “store‑and‑release” system, ensuring that maternal energy reserves are both built up and readily accessible when needed.
• Understanding these endocrine mechanisms provides a foundation for clinicians to interpret weight‑gain patterns, anticipate metabolic complications, and support healthy postpartum transitions.

By appreciating the hormonal choreography that underlies body‑composition changes, we gain a deeper, evergreen insight into the physiology of pregnancy—knowledge that remains relevant across populations, clinical settings, and evolving research landscapes.