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Background: The effect of a weight-loss intervention on the masses of lean tissues and organs in humans is not well known., Objective: We studied the effects of a diet and exercise weight-loss intervention on skeletal muscle (SM) mass and selected organs over 2 y using MRI in overweight adults with type 2 diabetes., Design: Participants were 53 women and 39 men [mean ± SD: age 58 ± 7 y; body mass index (BMI; in kg/m 2 ) 32 ± 3] enrolled in the Look AHEAD (Action for Health in Diabetes) trial and randomly assigned to an intensive lifestyle intervention (ILI) or diabetes support and education (DSE) on whom 2 y of data were collected. MRI-derived measurements of SM, heart, liver, kidney, spleen, and pancreas were acquired., Results: Adjusted for baseline weight, height, age, sex, and ethnicity, the ILI group weighed (mean ± SE) 6.6 ± 0.7 kg less after 1 y and 5.2 ± 0.7 kg less after 2 y, whereas the DSE group did not change significantly (-0.4 ± 0.6 and -1.0 ± 0.7 kg after 1 and 2 y, respectively; P-interaction < 0.001). Total SM decreased in both groups during year 1 (-1.4 ± 0.2 kg; P < 0.001) with appendicular SM regained during year 2. Liver and spleen masses decreased in the ILI group (-0.12 ± 0.02 and -0.006 ± 0.003 kg, respectively) but were unchanged in the DSE group (0.00 ± 0.02 and 0.004 ± 0.003 kg, respectively). Kidney mass decreased by 0.013 ± 0.003 kg (P < 0.001) over 2 y in both groups., Conclusions: Decreases in liver (in Caucasians but not African Americans) and spleen were detected after a 6.2-kg weight reduction compared with a control group. SM and kidney mass decreased in both groups. Appendicular SM was regained during the second year whereas trunk SM was not. No evidence of a disproportionate loss of high-metabolic rate organs (heart, liver, kidney, spleen) compared with SM was found., (© 2017 American Society for Nutrition.)

The question of whether parenteral nutrition adversely affects calcium regulation remains unclear. Human studies of this question have been confounded by uncontrolled variables including the degree to which food is ingested orally; gut absorption; underlying disease; medication adversely affecting bone, including steroids; and aluminum contamination of parenteral nutrients. The present study was undertaken to examine whether parenteral nutrition adversely affects calcium regulation in a nonhuman primate model that allows for control of underlying clinical variables and mobility. With use of this model, it was possible to show weight maintenance and positive nitrogen and calcium balances with parenteral nutrition. There was no demonstrable effect of the animals' wearing a jacket and tether system or of catheterization on calcium regulation. Calciuria in response to parenteral nutrition was elevated initially but diminished by 2 wk of therapy. The calciuria observed resulted from an increased urine-filtered calcium load. Calcium balance with parenteral nutrition was preserved by a diminished fraction of calcium filtered by the kidney being excreted in the urine. The present study suggests that negative calcium balance produced by parenteral nutrition may result from abnormal renal tubular function or disruption of normal parathyroid hormone regulation.

The etiology of bone disease seen in long-term total parenteral nutrition patients is poorly defined. This study examined the question of whether abnormal bone could be induced in otherwise normal weanling rats fed a balanced nutrient solution intravenously. Young adult, male Wag/Rij rats were divided into three groups. One group was fed a commercial liquid research diet, one group received an indwelling jugular catheter and was fed an intravenous elemental solution formulated to be nutritionally complete, and one group received an indwelling catheter but was fed the commercial liquid diet orally. Significant differences were seen between groups in percent bone, femur length, growth-plate width, endosteal label area, periosteal mineral apposition rate, and periosteal and endosteal bone-formation rates. This study suggests that intravenous administration of otherwise adequate nutrients to rats results in altered bone remodeling compared to orally fed cohorts.

A freely mobile jacket and tether system was developed for the investigation of total parenteral nutrition (TPN)-induced metabolic bone disease and complications of prolonged TPN in 12 Macaca fascicularis nonhuman primates. The animals received TPN for 49 +/- 7 d (means +/- SEM), providing 82 +/- 2 kcal.kg-1.d-1. Serum glucose increased from 3.6 +/- 0.2 mmol/L at baseline to 8.3 +/- 1.9 mmol/L (p less than 0.01) during TPN, and serum albumin decreased from 38 +/- 1 g/L at baseline to 29 +/- 1 g/L (p less than 0.001) during 2.75% amino acid TPN and 30 +/- 2 g/L (p less than 0.01) during 5% amino acid TPN infusion. No significant changes were seen in serum prealbumin, total protein, bilirubin, alanine aminotransferase, and 5'-nucleotidase during TPN infusion. Major complications included catheter sepsis, hyperglycemia, diarrhea, and premature death in six animals. Thus, metabolic complications of prolonged TPN support may be investigated in a freely mobile nonhuman primate.

The impact of parenteral nutrition on mineral loss was examined in 11 long-term (10-79 mo) and 6 short-term (1-8 mo) patients. In the long-term patients, there was a significant (p less than or equal to 0.02) urinary loss of calcium and magnesium during infusion compared with periods off infusion. The magnitude of urinary excretion of these minerals was much lower than in previously reported series and in short-term patients. Despite this, in long-term patients the mean bone mass at the spine was lower than normal (p less than 0.001) but mean bone mass at the wrist was not. Current data suggest that hypercalciuria is not a consistent feature of parenteral nutrition. Furthermore, osteopenia is a feature of some long-term parenteral nutrition patients.

The characteristics of bone disease associated with parenteral nutrition are controversial. To further elucidate the contribution of aluminum deposition to this syndrome and the spectrum of pathology in patients supported by current regimens utilizing crystalline amino acids, quantitative histomorphometry and staining for Al were performed on iliac crest bone biopsies from 26 long-term parenteral nutrition patients and 16 normal volunteers. Compared with normal subjects, median trabecular bone area (TBA) for a group with positive Al staining (n = 14) who were exposed to casein hydrolysate was significantly less (12.9% vs 20.7, p less than 0.05) as was the median rate of bone formation (RBF) (29 micron2 X mm-2 X d-1 vs 360, p less than 0.05). A variety of abnormal histological findings were present in patients without positive aluminum stains (n = 12) who were supported solely by regimens utilizing crystalline amino acids. However, neither decreased TBA (median TBA = 15.3%) nor decreased RBF (median RBF = 126 micron2 X mm-2 X d-1) was uniformly characteristic of the latter patient group.