Low birth weight (LBW) infants have higher risk of developing insulin resistance and its comorbidities later in life. The concept of “developmental origins of health and disease” suggests that intrauterine and postnatal environments have an important role in increasing these risks. The risk of such adult-onset diseases in LBW infants might be associated with adipose tissue maldevelopment including altered body composition and increased amount of visceral fat, which is the same mechanism as that in children and adults with metabolic syndrome. However, LBW infants often have different characteristics: they are not always overweight or obese over their life course. The inconsistency might be associated with the thrifty phenotype, which is produced in response to impaired growth potential and decreased lean body mass. LBW infants tend to be obese within the limits of impaired growth potential. Through our previous investigations evaluating longitudinal changes in adiponectin levels at an early stage of life, we speculated that probably, the intrauterine life of term infants or the period up to term-equivalent age in preterm infants might be the key age for the development of adipose tissues including fat cells. Because of that, we hypothesized that the smaller number of adipocytes in LBW infants might be associated with overloading of single adipocytes and impaired adipose tissue expandability. The possible mechanisms are discussed from the perspective of adipose tissue maldevelopment in LBW infants.