Protein Deficit Research Articles

Rumen Fermentation and Nitrogen Balance of Lambs fed Diets Containing Plant Extracts Rich in Tannins and Saponins, and Associated Emissions of Nitrogen and Methane

Tannins were added to experimental diets at levels of 1 and 2g/kg DM (hydrolysable tannins; Castanea sativa wood extract) and saponins at 2 and 30mg/kg DM (sarsaponin; Yucca schidigera extract). These levels were far below thresholds expected to be adverse in ruminants. Effects were measured in lambs by comparison with unsupplemented control diets calculated to be either deficient (10%) or adequate in protein. The diets consisted of hay, concentrate (1:1) and extra wheat starch with increasing body weight. Ruminal pH, VFA concentration, protozoa count and apparent digestibilities of organic matter and fibre did not differ among treatments. The low tannin dose significantly decreased bacteria count compared to the high saponin dose. Saponin supplementation and the high tannin dose showed some potential to reduce ruminal ammonia concentration. This was associated with weak trends towards lower urine N excretion (only tannins) and ammonia emission from manure. Methane release was increased by the low tannin dose compared to the unsupplemented control. Diet effects on heat production were not systematic. In conclusion, the extracts rich in tannins or saponins gave only slight indications for either increased body nitrogen retention or reduced nitrogen emission. However, effects might have been larger with more pronounced dietary protein deficit.

The Capacity of Noninflammatory (Steady-State) Dendritic Cells to Present Antigen in the Primary Response Is Preserved in Acutely Protein- or Energy-Deficient Weanling Mice

The objective of this investigation was to determine the influence of wasting protein and/or energy deficits on the capacity of dendritic cells to initiate primary responses. Weanling male and female C57BL/6J mice were permitted free access to a complete purified diet, free access to an isocaloric low protein purified diet (combined deficiencies of protein and energy) or restricted intake of the complete diet (energy deficiency) for up to 14 d; a 19-d-old zero-time control group was also included. Malnourished mice lost 1.5-2% of initial body weight daily. Antigen presentation by dendritic cells from spleen and lymph nodes was assessed in vitro by the primary one-way allogeneic mixed lymphocyte reaction using CBA/J mononuclear or CD4(+) T cells as responders. This function was sustained despite advanced weight loss and, remarkably, was increased in cell suspensions from 14-d energy-deficient mice. Antigen presentation by dendritic cells in mononuclear suspensions was examined in vivo using the host-vs.-graft response in CBA/J recipients, and an ontogeny-related increase was sustained in both malnourished groups through 14 d of weight loss. Neither wasting protocol influenced the proportion of mononuclear cells (1-2%) exhibiting dendritic cell phenotype (CD11c(+)F4/80(-/low)) in the cellular suspensions used to study antigen-presenting activity. Consequently, these functional studies are interpretable on a per dendritic cell basis. In the absence of infectious or inflammatory pressure, the dendritic cell retains antigen-presenting capacity despite acute (wasting) deficiencies of protein and/or energy. The results are relevant to presentation of both foreign (adjuvant role) and self (tolerizing role) antigens by the dendritic cell.

Contrast in adaptive mass gains: Eurasian golden plovers store fat before midwinter and protein before prebreeding flight.

Before predictable periods of high nutritional demand and little or no intake, vertebrates store fuel mainly composed of energy-dense lipids or energy-poor but protein-rich muscle tissue. Documenting contrasts in fuel composition and storage patterns within species, or even within individuals, would greatly help to elucidate the functional significance of the variety of storage strategies demonstrated in birds. We show here that the 40-50 g mass gain of 200 g in Eurasian golden plovers (Pluvialis apricaria) in autumn in The Netherlands consists of fat only, but that the similar gain in body mass in spring consists of proteinaceous tissue (pectoral and other skeletal muscle and possibly skin tissue). That the same golden plovers store energy in autumn and store protein in spring suggests that they face energy deficits in early winter and risk protein deficits in spring, especially perhaps after arrival on the breeding grounds in late April and early May. In autumn and winter their diet consists largely of protein-rich earthworms, but upon arrival on Low Arctic and montane tundras, golden plovers tend to eat berries which are rich in sugars but notably poor in proteins. We therefore propose that the build-up of proteinaceous tissue in spring reflects a strategic storage of a nutritional resource that is likely to be in short supply somewhat later in the year.

Identification of genes enhanced by protein-calorie malnutrition by differential display polymerase chain reaction (expression of fibrinogen B beta chain, B cell translocation gene 1 and thyroid hormone responsive protein genes).

Protein-calorie malnutrition (PCM), as one of global health problems, arises during protein and/or energy deficit due to disease and nutritional inadequacy. Previously, we showed that PCM elicited oxidative stress with activation of the phase II detoxifying gene expression, which was reversed by cysteine supplementation. As part of the attempts to identify the cellular adaptive responses and the associated gene expression during PCM, the current study was initiated to analyze the genes differentially expressed in the rat during PCM. Among 1,916 bands amplified, 85 putative differentially amplified bands were enhanced by PCM in the liver, while the expression of 64 bands was suppressed. Northern and/or reverse transcription-polymerase chain reaction (RT-PCR) analyses revealed that PCM increased the expression of fibrinogen B beta chain, B cell translocation gene I (BTGI) and thyroid hormone responsive protein (THRP) mRNAs. The increase in the hepatic fibrinogen B beta chain mRNA was not prevented by cysteine supplementation, whereas cysteine decreased the enhancement in the rGSTA2 and microsomal epoxide hydrolase mRNA expression. Cysteine was also active in reversing the increase in BTG1 mRNA during PCM. This was supported by the increase in BTG1 mRNA in H4IIE cells exposed to sulfur amino acid-deprived medium. Northern blot analysis revealed that THRP, highly expressed in the brain in a tissue-specific manner, was induced by PCM and that cysteine supplementation abolished the THRP induction. Conversely, the level of hepatic albumin mRNA was markedly decreased by PCM, which was partially restored by cysteine supplementation. Differential display RT-PCR analysis allowed us to identify the genes that are responsive to oxidative stress during PCM and to characterize the differential role of cysteine on the expression of the fibrinogen B beta chain, BTG1 and THRP genes as a homeostatic adaptive response during protein deficiency.

Insights into the Abnormalities of Chronic Renal Disease Attributed to Malnutrition

ABSTRACT. Low values of serum proteins and loss of lean body mass are commonly found in patients with chronic renal insufficiency (CRI) and especially in dialysis patients. These abnormalities have been attributed to malnutrition (i.e., an inadequate diet), but available evidence indicates that this is not the principal cause. In contrast, there is persuasive evidence that secondary factors associated with the CRI condition cause abnormalities in protein turnover and ultimately result in low serum protein levels and loss of lean body mass. Recent reports have identified some factors that could interfere with the control of protein turnover in CRI patients, including acidosis, inflammation, and/or resistance to anabolic hormones. Each of these stimulates protein breakdown in muscle and activates a common proteolytic pathway, the ubiquitin-proteasome pathway. Moreover, acidosis or inflammation suppress hepatic albumin synthesis. Understanding the biochemical mechanisms that regulate the ubiquitin-proteasome and other catabolic pathways are required to identify new strategies for preventing protein deficits that are associated with CRI.

Postnatal malnutrition and growth retardation: an inevitable consequence of current recommendations in preterm infants?

Nutrient intakes meeting recommended dietary intakes (RDIs) take time to establish and once established are rarely maintained throughout hospital stay in preterm infants. A nutrient deficit, therefore, accrues. RDI are based on needs for maintenance and growth, with no provision to replace this deficit. We, therefore, hypothesized that postnatal malnutrition and growth retardation were inevitable in infants fed current RDI. Dietary intakes were prospectively collected, by a single observer (N.P.), on a daily basis in a group of preterm infants (n = 105; birth weight </=1750 g; gestational age </=34 weeks) admitted to neonatal intensive care unit over a 6-month period. Actual was subtracted from recommended energy (120 kcal/kg/day) and protein (3 g/kg/day) intakes and nutritional deficits calculated. Infants were weighed on admission and throughout hospital stay. The data were analyzed using a combination of repeated measures analysis of variance and stepwise regression analysis. Nutrient intakes meeting current RDIs were rarely achieved during early life. By the end of the first week, cumulative energy and protein deficits were 406 +/- 92 and 335 +/- 86 kcal/kg and 14 +/- 3 and 12 +/- 4 g/kg in infants </=30 and those at >/=31 weeks. By the end of the fifth week, cumulative energy and protein deficits were 813 +/- 542 and 382 +/- 263 kcal/kg and 23 +/- 12 and 13 +/- 15 g/kg and the z scores were -1.14 +/-.6 and -.82 +/-.5 for infants at </=30 and >/=31 weeks. Stepwise regression analysis indicated that variation in dietary intake accounted for 45% of the variation in changes in z score. Preterm infants inevitably accumulate a significant nutrient deficit in the first few weeks of life that will not be replaced when current RDIs are fed. This deficit can be directly related to subsequent postnatal growth retardation.postnatal growth retardation, preterm infants.

Scanning electron microscopy of rat erythrocytes during chronic alcoholic intoxication combined with protein and vitamin deficit.

Electron microscopy revealed morphological changes in erythrocytes from rats with chronic alcoholic intoxication kept on protein- and vitamin B-deficient rations. All animals had anisopoikilocytosis (up to 50%). Most pronounced changes in erythrocyte population attesting to accelerated erythrocyte aging (stomato- and microcytosis, discocyte swelling, and spontaneous hemolysis) were found in alcohol-fed rats kept on deficient ration.

Activity of Digestive Enzymes in Small Intestine in Rat Pups Whose Mothers Were Kept on Low-Protein Diet during Pregnancy and Lactation

Nutrition of mother and offspring plays an important role in formation of enzyme spectrum in small intestine of developing organism. We have obtained different results with respect to effects of protein deficit in maternal nutrition during pregnancy and lactation on formation of different enzyme systems in offspring, which provide membrane and intracellular digestion. In some cases, the maximal changes of enzyme activities were found in the rat pups kept on a low-protein diet during the embryonic development (saccharase, dipeptidase), in other cases, in the rat pups on such nutrition at the period of early postnatal development (alkaline phosphatase). In the third case, the changes were practically the same for the both groups of animals (maltase).

Prevention of c-Jun/activator protein-1 activation and microsomal epoxide hydrolase induction in the rat liver by cysteine during protein–calorie malnutrition

Protein–calorie malnutrition (PCM), a major global health problem, arises during protein and/or energy deficit due to disease and nutritional inadequacy. To date, cellular adaptive responses and gene expression associated with PCM remain poorly understood. In view of the primary role of the liver in energy conversion, the present study was designed to investigate changes in hepatic morphology and molecular alterations during PCM. PCM caused marked decreases in the cytoplasmic eosinophilic content and nuclear shrinkage in the hepatocytes with a decrease in glutathione content. The nuclear activator protein-1 (AP-1) complex was activated in the liver of PCM rats. AP-1-binding activity of nuclear extracts produced from PCM rats was reduced by the presence of anti-c-Jun antibody. Microsomal epoxide hydrolase (mEH), a phase II detoxifying enzyme, was 4-fold induced, with a 20-fold increase in the mRNA level during PCM. In contrast to the PCM-induced changes in hepatic morphology, PCM rats supplemented with cysteine showed an increase in the GSH level and well-preserved hepatic structures with mild fat degeneration. Cysteine supplementation inhibited the activation of AP-1 and the induction of mEH in PCM rats. These results provided evidence: (i) that PCM alters liver morphology with a decrease in the glutathione level; (ii) that cysteine may serve as a key element responsible for preserving hepatic morphology and maintaining the glutathione level; and (iii) that cysteine was active in preventing the activation of AP-1 and mEH induction in the liver during PCM.

Body conditions scores of dairy cattle in organic farms

SummaryDairy cows on organic farms may not be fed adequately because provision of concentrates (and thus energy and protein), minerals and vitamins is limited. The hypothesis was therefore tested that the nutritional status of dairy cows in organic dairy production is insufficient. The nutritional status was characterized by determination of body conditions scores (BCS) in 152 farms, which were a stratified sample of Swiss organic farms. In summer (July – September 1997) and the ensuing winter (January – March 1998) the BCS was evaluated in 1687 and 1867 dairy cows, respectively. Mean number of cows per farm was 12.3, 13.7% of farms were located in mountain zones and 26% in lowlands, and 26% of farms kept part or all of their herds on alpine pastures during summer. Average 305‐day milk yield was 5467 kg per lactation. Depending on breed, this was 5–12% less than the contemporary average annual milk yield of cows registered in herd books. Average milk protein and fat contents were lower than that of cows kept on conventional farms. Mean milk urea concentration was 3.2 mmol/l in summer and only 2.0 mmol/l in winter, indicating insufficient protein supply in winter. BCS were between 3.0 and 3.75 for 69% of the cows, and &lt; 2 and &gt; 4 for 3 and 4% of cows, respectively. Effects on BCS of cow characteristics (days post‐partum, age and breed) and effects of farm characteristics with emphasis on feeding procedures were assessed with linear models. Days post‐partum, breed and several farm level variables had a significant influence on BCS. In conclusion, most dairy cows on organic farms had opitimal BCS and thus an adequate nutritional status. However nutritional energy and/or protein deficits were apparent during the winter feeding period

Total body protein in chronic diseases and in aging.

Substantial losses of total body protein (TBP) can occur in chronic diseases and in aging. Such losses impact negatively on immunity and quality of life, and on growth rates in children. Direct measurements of total body nitrogen (TBN) monitor the integrated changes in TBP over time and allow comparison with normal subjects. TBN assessment via neutron capture analysis is therefore the gold-standard method of TBP estimation, so that risk factors for protein deficit can be identified and patient management optimized. The nitrogen index (NI) can be used to predict prognostic outcome: an NI < 0.9 is associated with substantial wasting in HIV disease, an NI < 0.8 predicts significant pathophysiology in chronic renal failure, and a low NI is predictive of neutropenia in breast-cancer patients. These findings emphasize the central importance of adequate protein stores in recovery from disease or in maintaining quality of life. Aging appears to involve a gradual loss of TBP throughout adulthood. Cross-sectional data suggest that TBP declines curvilinearly with age, such that there is an accelerated decline after 65 years of age. However, longitudinal data are scarce, and little is known about the relative loss of visceral protein, as opposed to skeletal muscle protein. More clearly-defined data are essential if the effects of aging per se are to be separated from the effects of chronic disease. A further complication is the knowledge that physical activity also declines with age. Thus sarcopenia, the loss of skeletal muscle mass, could primarily result from disuse rather than aging. The economic impact of unsuccessful aging places a pressing need for multicompartment data in longitudinal study designs.

Effects of cowpea (Vigna Unguiculata) feeding on the pancreatic exocrine secretion of pigs

Introduction Cowpea (Vigna unguiculata) is a valuable protein source that can contribute towards overcoming a predicted protein deficit equivalent to more than 1 000 000 t oilcake in Southern Africa by the year 2000 (Nell et al. 1992). However, like most other legumes, cowpeas contain antinutritional factors (ANFs) (Makinde et al. 1996). It has also been shown that feeding raw cowpea causes reduced growth and histomorphometric changes in the various segments of the intestine (Makinde et al. 1997) attributable to ANFs. The major ANFs in the cowpea are trypsin inhibitors, tannins and phytates (Aletor and Aladetimi 1989). Although the protease inhibitors are found in most legumes, only soybean inhibitors have been thoroughly investigated (Liener and Kakade 1980), and trypsin inhibitors in other legumes have received little attention.

Energy and nutrient status of amenorrheic athletes participating in a diet and exercise training intervention program.

Chronic energy deficit is one of the strongest factors contributors to exercise-induced menstrual dysfunction. In such cases, macro- and micronutrient intakes may also be low. This study presents the results of a diet and exercise training intervention program. designed to reverse athletic amenorrhea, on improving energy balance and nutritional status in 4 amenorrheic athletes. The 20-week program provided a daily sport nutrition supplement and 1 day of rest/week. The program increased protein intakes for the 3 athletes with a protein deficit to within the recommended levels for active individuals. Micronutrient intakes increased, as did serum concentrations of vitamin B12, folate, zinc, iron, and ferritin. These results indicate that some amenorrheic athletes have poor nutritional status due to restricted EIs and poor food selections. A sport nutrition supplement may improve energy balance and nutritional status in active amenorrheic women.

Hepatic expression of growth hormone receptor/binding protein and insulin-like growth factor I genes in uremic rats. Influence of nutritional deficit.

The molecular basis for GH resistance in chronic renal failure is unknown. It may partly reside in a decreased number of hepatic GH receptors and subsequently reduced IGF-I synthesis. To investigate the hepatic expression of GH receptor/binding protein (GHBP) and IGF-I genes in chronic renal failure, mRNA levels and the concentrations of its splicing variants were measured by Northern Blot in male 5/6 nephrectomized rats (NX, n = 9), aged 26 +/- 1 days, and three groups of sham-operated rats: (1) fed ad libitum (SAL, n = 9); (2) pair-fed with NX (SPF, n = 7); and (3) pair-fed with NX in terms of protein ingestion but calorically supplemented up to the intake of SAL (SPF+, n = 8). NX rats had severe renal failure, serum urea nitrogen 106 +/- 11 mg/dl (mean +/- SEM), and were growth retarded. GH receptor/GHBP gene expression was detected as two bands of 4.7 and 1.2 kb, respectively. The amount of mRNA was lower (P < 0.0001) in NX than SAL, either when both bands were considered together or separately. No differences were found between NX, SPF, and SPF+. Serum GHBP concentrations were higher (P < 0.01) in NX rats than the other groups. For the IGF-I gene, two bands of 7.5 and 1.8-0.8 kb were identified. Expression of IGF-I gene was reduced (P < 0.05) in NX in comparison with SAL, this reduction being more marked for the 7.5 kb transcript (amount of mRNA equal to 56.6 +/- 2.6 vs 84.8 +/- 6.2% of values found in SAL rats). There were no differences between NX and SPF. Normalization of caloric intake in SPF+ resulted in partial recovery of the 7.5-kb band and did not modify the 1.8-0.8 kb mRNAs. Circulating IGF-I levels were no different among the four groups. These data confirm that expression of liver GH receptor/GHBP and IGF-I genes is markedly decreased in uremic rats. Nutritional deficiency and not uremia itself seems to be the main causal factor, with protein deficit playing a major role.

Molecular mechanisms of copper metabolism and the role of the Menkes disease protein.

Menkes disease is an X-linked, recessive disorder of copper metabolism that occurs in approximately 1 in 200,000 live births. The condition is characterized by skeletal abnormalities, severe mental retardation, neurologic degeneration, and patient mortality in early childhood. The symptoms of Menkes disease result from a deficiency of serum copper and copper-dependent enzymes. A candidate gene for the disease has been isolated and designated MNK. The MNK gene codes for a P-type cation transporting ATPase, based on homology to known P-type ATPases and in vitro experimentation. cDNA clones of MNK in Menkes patients show diminished or absented hybridization in northern blot experiments. The Menkes protein functions to export excess intracellular copper and activates upon Cu(I) binding to the six metal-binding repeats in the amino-terminal domain. The loss of Menkes protein activity blocks the export of dietary copper from the gastrointestinal tract and causes the copper deficiency associated with Menkes disease. Each of the Menkes protein amino-terminal repeats contains a conserved -X-Met-X-Cys-X-X-Cys- motif (where X is any amino acid). These metal-binding repeats are conserved in other cation exporting ATPases involved in metal metabolism and in proteins involved in cellular defense against heavy metals in both prokaryotes and eukaryotes. An overview of copper metabolism in humans and a discussion of our understanding of the molecular basis of cellular copper homeostasis is presented. This forms the basis for a discussion of Menkes disease and the protein deficit in this disease.

Dietary Carbohydrate and Fat Do Not Alter the Thyroid Response to Protein Deficiency in Chicks

Consumption of low-protein diets consistently causes elevations in circulating levels of triiodothyronine (T3) in several species of animals. In chicks this is often accompanied by lower levels of circulating thyroxine (T4). Since low-protein diets are usually formulated by replacing the detected protein with carbohydrate, the question arises as to whether the changes in thyroid hormones are a result of the lower protein or higher amounts of carbohydrate in such diets. Male broiler chicks, 13-26 days of age, were fed experimental diets that contained either an adequate level of protein (24%) or levels that were slightly (17%) or moderately (10%) deficient in protein. The deleted protein was replaced, isocalorically, with either glucose, soybean oil, or hydrogenated coconut fat. Though the level of protein and source of energy differed among diets, all diets contained identical amounts of all nutrients and energy, and were of similar weight densities. Circulating levels of thyroid hormones were measured from blood samples taken at the end of the study. Plasma T3 was elevated to a similar degree in all protein-deficient animals compared with control. Plasma T4 decreased in all protein-deficient chicks and was lowest with 10% dietary protein. Changes in circulating levels of thyroid hormones occurred independently of the source of dietary energy. Therefore, it is concluded that alterations in circulating levels of thyroid hormones that occur in chicks fed low-protein diets are a specific effect of the protein deficit and are not a related to the amounts of carbohydrate or fat present in the diet.

Gender Affects Rats' Central Nervous System Histaminergic Responses to Dietary Manipulation

The histaminergic system (histamine and its H1-receptor) of the central nervous system has been implicated in control of food intake. The reported studies were designed to examine the effects of food restriction and very low (1%) protein diets on central nervous system H1-receptors in male and female rats. In a series of experiments, groups of rats were freely fed a 25% protein diet, a 1% protein diet, or fed the 25% protein diet at 4 g/100 g body weight for 14–20 d. When freely fed 25% protein diets, females had higher whole-brain H1-receptor binding than males on d 1 (female 122.36 ± 4.53 and male 65.78 ± 3.82 pmol/g protein; P < 0.001). Changing diets affected central H1-receptor binding in both males and females (P < 0.003). When rats were fed both restricted levels of food and 1% protein diets, the receptor binding of males increased by d 5 whereas that of females decreased by d 5 (P < 0.001). When fed 1% protein diets, females had decreased H1-receptor binding (98.4 ± 2.38 pmol/g protein) and that in males increased to 119.81 ± 5.09 pmol/g protein. After 15 d, females had eaten significantly more food than males: females 166 ± 4.9 g, males 124 ± 1.9 g (P < 0.0007). Males had a significantly greater weight loss than females: males -28.8 ± 2.6 g, females -17.08 ± 0.97 g (P < 0.0007). When fed restricted diets, females had decreased H1-receptor binding (93.81 ± 5.58 pmol/g) whereas binding in males increased to 111.27 ± 8.55 pmol/g. Preliminary saturation binding studies indicated that restricted food intake lowered receptor density (females consuming 25% protein: 715 ± 30 pmol/g protein; female restricted: 467 ± 28 pmol/g protein, P < 0.05), while 1% protein increased receptor sensitivity, i.e., lowered KD (males consuming 25% protein: 15.3 ± 1.8 nmol; males fed low protein: 2.8 ± 0.27 nmol). This study suggests that dietary manipulation affects central H1-receptor binding in a gender-specific manner, thereby modulating central histaminergic activity during food or protein deficit.

The specific locus and time course of the body protein adjustments produced in rats by lesions of the lateral hypothalamus

Lesions of the lateral hypothalamus (LH) result in a body weight reduction characterized by declines in both lean and adipose tissues. The body fat of LH-lesioned rats can be restored to or above the levels of nonlesioned rats by overfeeding. However, the protein deficit cannot be so reversed, suggesting that the lesion-induced body protein reduction is chronic. To ascertain which specific tissues surrender protein following LH lesions, the present studies measured skeletal muscle and visceral organ weights at 2 weeks and 6 months postlesion. Daily protein losses during the first 2 weeks postlesion were also assessed to determine the temporal pattern of whole-body protein adjustments. The results at 6 months postlesion suggest that LH lesions lead to reductions in the maintained mass of all protein-based tissues. The largest absolute loss was from skeletal muscle, whereas liver sustained the greatest proportional loss. Assessment of daily postlesion protein balance indicate that the majority of body protein losses occurred during the initial 6 days postlesion. Skeletal muscle mass was characterized by large losses at 2 weeks, and proportionally smaller losses at 6 months. Reductions of visceral organ mass were marginal at 2 weeks, but substantial by 6 months postlesion. Thus, whereas all protein-based tissues are reduced by LH lesions, the protein content of specific tissues appears to be altered differentially. Major reductions in total body protein occur in the first 2 weeks of the LH syndrome, with an apparent redistribution of protein later. This redistribution results in the partial restoration of skeletal muscle at the expense of existing visceral organ protein or its subsequent accretion.

Small bowel necrosis associated with postoperative jejunal tube feeding CD SCHUNN, JM DALY University of Pennsylvania School of Medicine, Philadelphia

Small bowel necrosis associated with postoperative jejunal tube feeding CD SCHUNN, JM DALY University of Pennsylvania School of Medicine, Philadelphia

A Comparison of Photosynthate Allocation in Lakes

We compared the relationships between photosynthate allocation to protein, carbohydrate, lipid and low molecular weight (LMW) fractions and the variables daylength and water temperature in Lakes Huron, Michigan, and Ontario as well as three smaller headwater lakes in the Lake Ontario drainage. In all lakes investigated the allocation of recently produced photosynthate to carbohydrate was strongly related to daylength (% carbohydrate = −3.5 * daylength (hr) + 72.8; n = 59, r 2 = 0.56). The percentage of photosynthate allocated to protein was a function of water temperature in all lakes although the y-intercept for the protein-temperature relationship was much lower in the three headwater lakes and Lake Ontario (% protein = 0.50 * temperature (°C) + 6.1; n = 37, r 2 = 0.52) than in Lake Huron and Lake Michigan (% protein = 0.68 * temperature (°C) + 24.2; n = 23, r 2 = 0.49). The increase in allocation to protein was related to a decrease in allocation to low molecular weight material (% LMW = −1.1 * % protein + 57.13; n = 60, r 2 = 0.72). The percentages of photosynthate in lipid and LMW material were not related to any of the environmental variables measured. Assuming that photosynthate allocation is related to biochemical composition, the phytoplankton in Lakes Huron and Michigan were more protein rich for a given temperature than those in Lake Ontario and in the smaller inland lakes. The protein deficit was due to an increase in allocation to LMW material.